6 Farming human pathogens

6

Farming human pathogens

Here we examine examples of the farming of coevolutionary systems, focusingon the mutually amplifying roles of large-scale psychosocial stress, economicstructure, and reductionist interventions in the ecology and evolution of highlyadaptive disease organisms. We find, in general, that population-level socioe-conomic and other stressors, in synergism with reductionist interventions,are precisely suited to trigger mesoscale resonance coevolutionary resiliencedomain shifts affecting rapidly evolving pathogens. In an ideal world thesechanges would be the deliberate alteration of socioeconomic structure aimedat decreasing rates of infection and/or virulence, perhaps extending the util-ity of reductionist intervention. These case histories examine exactly contrarypatterns.

6.1 Culture and the infection phenotype: a modelingexercise

Taking the perspectives of the earlier chapters, we can begin to model howpopulation-directed, structured, psychosocial stress imposes an image of itselfon the coevolutionary conflict between a highly adaptive chronic infection andthe immune response.

As population-level structured stress appears a fundamental part of thebiology of disease in human populations, this suggests the possibility that sim-plistic individual-oriented magic-bullet drug treatments, vaccines, and risk-reduction programs that do not address the fundamental living and workingconditions which underlie disease ecology will fail to control many current epi-demics. In addition, such reductionist interventions may go so far as to selectfor more holistic pathogens characterized by processes operating at multiplelevels of biocultural organization.

R. Wallace et al., Farming Human Pathogens, DOI 10.1007/978-0-387-92213-3_6, © Springer Science+Business Media, LLC 2009

110 6 Farming human pathogens

6.1.1 Introduction

Earlier work in this direction (Wallace and Wallace, 2002; Wallace, 2002a)examined culturally-driven variation in HIV transmission and malaria pathol-ogy. HIV responds to immune challenge as an evolution machine, generatingcopious variation and hiding from counterattack in refugia at multiple scales ofspace, time, and population. P. falciparum engages in analogous rapid clonalantigenic variation, and cyto-adherence and sequestration in the deep vascu-lature, primary mechanisms for escaping from antibody-mediated responsesof the host’s immune system (Alred, 1998). Something much like the mutatorphenotype (Thaler, 1999) or second order selection (Tenallion et al., 2001),by which the mechanisms mutations come about are themselves subjected toselection, appears to generate antigenic variation in the face of immune at-tack for a large class of pathogens. This could well be another version of theBaldwin effect.

Concomitantly, DiNoia and Neuberger (2002) outline the mechanismsby which the immune system’s own antibody-producing B-cells engage in asecond-order fine tuning of antibody production through somatic hypermuta-tion, allowing organisms to respond quickly and effectively to pathogens thatthey have been exposed to previously (Gearhart, 2002).

Many chronic infections, particularly pathogens that cloak themselves inantigenic coats of many colors, are very often marked by distinct stages overthe course of disease. HIV infections typically involve an initial viremia trigger-ing an immune response that drives the virus into refugia during an extendedasymptomatic period which, with the collapse of the immune system, endsin AIDS. Malaria’s most evident stages are expressed as explosive outburstsof rapid parasite replication that facilitate insect-mediated transmission be-tween hosts. HIV, malaria, and a third disease, tuberculosis, account for overfive million deaths a year worldwide and exemplify the evolutionary successof multiple-stage chronicity as a life history strategy (Ewald, 2000; Villarreal,et al., 2000).

Here we analyze how pathogen life history stages represent a kind of co-evolutionary punctuation for chronic infection in the face of relentless immuneand other selection pressures. For HIV that punctuation may arise from thedirect interactions between the virus and the immune system response. In thecase of malaria, it may result by means of a second order punctuation throughthe mutator mechanism (Thaler, 1999) associated with rapid antigenic varia-tion. Elsewhere we have studied clonal selection in tumorigenesis from such asecond order perspective (Wallace et al., 2003).

How can we characterize the interpenetration between antagonistic adap-tive processes that defines disease dynamics? As described earlier, Adami etal. (2000) applied an information theoretic approach to conclude that genomiccomplexity resulting from evolutionary adaptation can be identified with theamount of information a gene sequence stores about its environment. Lewon-tin (2000) suggested something of a reverse process, in which environmental

6.1 Culture and the infection phenotype: a modeling exercise 111

complexity represents the amount of information organisms introduce intotheir environment as a result of their collective actions and interactions. Wepropose modeling the interactions among information sources – generalizedlanguages – provides a more faithful encapsulation of the interactive, multi-scale nature of pathogen-immune dynamics than does the common differentialequation predator-prey paradigm (e.g., Nowak and May, 2000).

Characterizing information sources as able to reflect their own context, asAdami et al. mapped out, we have applied a rate distortion argument in thecontext of imposed renormalization symmetry to obtain evolutionary punc-tuated equilibrium, and can use the more general Joint Asymptotic Equipar-tition Theorem (JAEPT) to conclude that pathogenic adaptive response andcoupled cognitive immune challenge will be jointly linked in chronic infec-tion, and subject to a transient punctuated interpenetration very similar toevolutionary punctuation. Multiple punctuated transitions, perhaps of mixedorder, may well constitute shifts to the different stages of chronic infection.

Examining paths in parameter space for the renormalization propertiesof such transitions – the universality class tuning of chapter 3 – produces asecond order punctuation in the rate at which the selection pressure of theimmune system imposes a distorted image of itself onto pathogen structure.This is our version of the mutator or Tenallion et al.’s second order selection.

Recognizably similar matters have long been under scrutiny: interactionsbetween the central nervous system (CNS) and the immune system, and be-tween genetic heritage and the immune system have become academicallycodified through journals with titles such as Neuroimmunology and Immuno-genetics. Elsewhere (Wallace and Wallace, 2002) we introduced another com-plication by arguing that the culture in which humans are socially embeddedalso interacts with individual immune systems to form a composite entity thatwe labeled an immunocultural condensation (ICC). It is, we will argue here,the joint entity of immune, CNS, and embedding sociocultural cognition thatengages in orders of punctuated interpenetration with an adaptive chronicinfectious challenge. Similar arguments are already in the French literature(e.g., Combes, 2000).

Included among the most damaging cultural inputs on immune systemfunction are the long-term psychosocial stresses of war, oppression, and dis-crimination imposed by one population on another. If valid, the paradigm hasfundamental consequences for concepts of human biology. While Diamond(1997) and others (Crosby, 1986; Hughes,2001) popularized ecological expla-nations of human history, the paradigm presented here suggests investigationin something of the other direction, at the means by which human historyshapes biological ontogeny, often through punctuated processes of mesoscaleresonance.

The paradigm would appear to have practical implications as well. Inter-penetrations among pathogens, the immune system’s response, and the em-bedding culture in which individuals find themselves would greatly color thesuccess of the kinds of individual-level disease interventions largely pursued


today. Reductionist interventions – drug regimens, vaccines, risk reductionprograms – aimed at holistic diseases, defined by myriad processes operatingat multiple scales of time and space both within and without individuals, arelikely to fail. Furthermore, what successes reductionist interventions have hadagainst reductionist diseases may very well select for holistic diseases ableto dilute or deflect the effectiveness of interventions pursued at single scalesalone.

There are some general considerations. First, the information theory ap-proach we have adopted in this book is notorious for providing existence the-orems whose representation, to use physics jargon, is arduous. For example,although the Shannon Coding Theorem implied the possibility of highly ef-ficient coding schemes as early as 1949, it took more than forty years forpractical turbo codes to be created. The program we propose is unlikely to beany less difficult.

Second, we are invoking information theory variants of the fundamentallimit theorems of probability. These are independent of exact mechanisms,but, as necessary conditions, constrain the behavior of those mechanisms.For example, although not all processes involve long sums of independentstochastic variables, those that do, regardless of the individual variable distri-bution, collectively follow a Normal distribution as a consequence of the Cen-tral Limit Theorem. Similarly, the games of chance in a Las Vegas casino areall quite different, but nonetheless the success of strategies for playing themis strongly and systematically constrained by the Martingale Theorem, re-gardless of game details. Languages-on-networks and languages-that-interact,as a consequence of the limit theorems of information theory, will be subjectto necessary-condition regularities of punctuation and generalized Onsagerrelations, regardless of detailed mechanisms, as important as the latter maybe.

Finally, just as parametric statistics are imposed, at least as a first ap-proximation, on sometimes questionable experimental situations, relying onthe robustness of the Central Limit Theorem to carry us through, we willinvoke here a similar heuristic approach for the information theory limit the-orems we define.

We begin with a reiteration and reinterpretation of some results from chap-ter 3.

6.1.2 Universality class tuning

Here we again iterate the general argument of chapter 3 onto the processof phase transition itself, obtaining Tenallion’s second order selection – themutator – in a natural manner.

We suppose that a structured environment, which we take itself to bean appropriately regular information source Y – e.g., the immune system,or more generally, for humans the immunocultural condensation (ICC) – en-gages a modifiable system – e.g., a pathogen – through selection pressure.


The ICC begins to write itself on the pathogen’s genetic sequences or proteinresidues in a distorted manner permitting definition of a mutual informationI[K] splitting criterion according to the Rate Distortion or Joint AsymptoticEquipartition Theorems. K is an inverse coupling parameter between systemand environment. According to our development, at punctuation – near somecritical point KC – the systems begin to interact very strongly indeed, and wemay write, near KC , taking as the starting point the simple physical modelof section 3.4,

I[K] ≈ I0[KC −KKC

]α.

For a physical system α is fixed, determined by the underlying universalityclass. Here we will allow α to vary, and to itself respond explicitly to selectionpressure.

Normalizing KC and I0 to 1, we obtain,

I[K] ≈ (1−K)α.

(6.1)

To repeat, the horizontal line I[K] = 1 corresponds to α = 0, while α = 1gives a declining straight line with unit slope which passes through 0 at K = 1.Consideration shows there are progressively sharper transitions between thenecessary zero value at K = 1 and the values defined by this relation for0 < K,α < 1. The rapidly rising slope of transition with declining α is, weassert, of considerable significance.

Again, the instability associated with the splitting criterion I[K] is definedby

Q[K] ≡ −KdI[K]/dK = αK(1−K)α−1,

(6.2)

and is singular at K = KC = 1 for 0 < α < 1. And again we interpretthis to mean that values of 0 < α � 1 are highly unlikely for real systems,since Q[K], in this model, represents a kind of energy barrier for informationsystems.


On the other hand, smaller values of α mean that the system is far moreefficient at responding to the adaptive demands imposed by the embeddingstructured ecosystem, since the mutual information which tracks the matchingof internal response to external demands, I[K], rises more and more quicklytoward the maximum for smaller and smaller α as the inverse coupling pa-rameter K declines below KC = 1. That is, systems able to attain smallerα are more adaptive than those characterized by larger values, in this model,but smaller values will be hard to reach, and can probably be done so only atsome considerable physiological or other cost, an energy argument similar tothat of the previous chapter.

The more biologically realistic renormalization strategies given in chapter3 produce sets of several parameters defining the universality class, whosetuning gives behavior much like that of α in this simple example.

We can formally iterate the phase transition argument on this calculationto obtain our version of the mutator, focusing on paths of universality classes.

6.1.3 The adaptive mutator

Suppose the renormalization properties of a biological or social language-on-a network system at some ‘time’ k are characterized by a set of parametersAk ≡ αk1 , ..., αkm. Fixed parameter values define a particular universality classfor the renormalization. We suppose that, over a sequence of ‘times’, the uni-versality class properties can be characterized by a path xn = A0, A1, ..., An−1

having significant serial correlations which, in fact, permit definition of an adi-abatically piecewise memoryless ergodic information source associated withthe paths xn. We call that source X.

We further suppose, as described earlier, that external selection pressureis also highly structured – e.g., the cognitive immune system or, in humans,the ICC – and forms another information source Y which interacts not onlywith the system of interest globally, but specifically with its universality classproperties as characterized by X. Y is necessarily associated with a set ofpaths yn.

We pair the two sets of paths into a joint path, zn ≡ (xn, yy) and invokean inverse coupling parameter, K, between the information sources and theirpaths. This leads, by the arguments above, to phase transition punctuationof I[K], the mutual information between X and Y, under either the JointAsymptotic Equipartition Theorem or under limitation by a distortion mea-sure, through the Rate Distortion Theorem (Cover and Thomas, 1991). Theessential point is that I[K] is a splitting criterion under these theorems, andthus partakes of the homology with free energy density which we have invokedabove.

Activation of universality class tuning, our version of the mutator, thenbecomes itself a punctuated event in response to increasing linkage betweenorganism – the pathogen – and externally imposed selection or other pressure– responses of the ICC. Mutation rates become a function of the relationship


between the ICC and the pathogen, above and beyond environmental insultalone.

Thaler (1999) has suggested that the mutagenic effects associated witha cell sensing its environment and history could be as exquisitely regulatedas transcription. Our invocation of the Rate Distortion or Joint AsymptoticEquipartition Theorems in address of the mutator necessarily means thatvariation comes to significantly reflect the grammar, syntax, and higher orderstructures of the embedding processes. This involves far more than a simplecolored noise – stochastic excursions about a deterministic spine – and mostcertainly implies the need for exquisite regulation. Our information theoryargument here converges with Thaler’s speculation.

In the same paper Thaler further argues that the immune system providesan example of a biological system which ignores conceptual boundaries thatseparate development from evolution. While evolutionary phenomena are notcognitive in the sense of the immune system (Cohen, 2000), they may stillpartake of a significant interaction with development, in which the very re-productive mechanisms of a cell, organism, or organization become closelycoupled with structured external selection pressure in a manner recognizablyanalogous to ‘ordinary’ punctuated evolution.

That is, we argue the staged nature of chronic infectious diseases like HIVand malaria represents a punctuated version of biological interpenetration, inthe sense of Lewontin (2000), between a cognitive ‘immunocultural conden-sation’ and a highly adaptive pathogen. We further suggest that this punc-tuated interpenetration may have both first (i.e., direct) and second ordercharacteristics, involving cross interactions between direct cognitive effects ofthe immune system or immunocultural condensation, or, more generally, ofthe ICC and the mutator mechanisms of both the immune system and itspathogen targets.

Another path to the mutator might be through a second order iterationsimilar to that just above, but focused on the parameters defining the univer-sality class distributions of section 3.3.

6.1.4 Population stress and pathogen response

As we discuss elsewhere (Wallace and Wallace, 2002; Wallace, 2002a), struc-tured psychosocial stress directed at populations, by policy choice or as un-foreseen consequence, constitutes a determining context for immune cognitionor, more generally, the immunocultural condensation. We wish to analyze theway structured stress affects the interaction between the cognitive ICC andan adaptive mutator, the principal line of defense against the ICC for a largeclass of highly successful pathogens. To do this we must extend our theoryto three interacting information sources, briefly reiterating the argument ofSection 2.4.

The Rate Distortion and Joint Asymptotic Equipartition Theorems aregeneralizations of the Shannon-McMillan Theorem which examine the inter-


action of two information sources, with and without the constraint of a fixedaverage distortion. We conduct one more iteration, and require a generaliza-tion of the SMT in terms of the splitting criterion for triplets as opposed tosingle or double stranded patterns. The tool for this is at the core of whatis termed network information theory (Cover and Thomas, 1991, Theorem14.2.3), leading to equations (2.1) and (2.2). We briefly review that develop-ment.

Suppose we have three (adiabatically piecewise stationary) ergodic infor-mation sources, Y1, Y2 and Y3. We assume Y3 constitutes a critical embeddingcontext for Y1 and Y2 so that, given three sequences of length n, the probabilityof a particular triplet of sequences is determined by conditional probabilitieswith respect to Y3:

P (Y1 = y1, Y2 = y2, Y3 = y3) =

Πni=1p(y1i|y3i)p(y2i|y3i)p(y3i).

(6.3)

That is, Y1 and Y2 are, in some measure, driven by their interaction withY3

Then, as with previous analyses, triplets of sequences can be divided by asplitting criterion into two sets, having high and low probabilities respectively.For large n the number of triplet sequences in the high probability set will bedetermined by the relation (Cover and Thomas, 1992, p. 387),

N(n) ∝ exp[nI(Y1;Y2|Y3)],

(6.4)

where splitting criterion is given by equation (2.1),

I(Y1;Y2|Y3) ≡

H(Y3) +H(Y1|Y3) +H(Y2|Y3)−H(Y1, Y2, Y3).


We can then examine mixed cognitive/adaptive phase transitions analo-gous to learning plateaus (Wallace, 2002b) in the splitting criterion I(Y1, Y2|Y3),which characterizes the synergistic interaction between structured psychoso-cial stress, the ICC, and the pathogen’s adaptive mutator. These transitionsdelineate the various stages of the chronic infection, which are embodied inthe slowly varying APSE phase between transitions. Again, our results areclosely analogous to the Eldredge-Gould treatment of evolutionary punctu-ated equilibrium in evolution.

We can, if necessary, extend this model to any number of interacting in-formation sources, Y1, Y2, ..., Ys conditional on an external context Z in termsof a splitting criterion defined by equation (2.2):

I(Y1; ...;Ys|Z) = H(Z) +s∑j=1

H(Yj |Z)−H(Y1, ..., Ys, Z),

where the conditional Shannon uncertainties H(Yj |Z) are determined bythe appropriate direct and conditional probabilities.

6.1.5 The phenotype coevolution ratchet

We have so far focused this treatment on complex parasites such as malariawhich may have mutator mechanisms determining behavior of their antigenticcoat of many colors. A simplified analysis can also be applied directly to HIV,which, as a kind of evolution machine, seems to engage in endless, rapid,direct mutation, and, at broader temporal scales, recombination. The essentialargument regarding RNA viruses is that the high error rate inherent to viralreplication is very nearly the lowest possible energy state consonant withquasi-species survival, according to the rate distortion argument of chapter 5.Nonetheless, a virus does not exist alone. It functions in cooperation with, aswell as in conflict with, the host organism. Some RNA viruses, for examplepoliomylitus and measles, have high error rate replication, but a (nearly) fixedphenotype, permitting effective vaccination.

The development of Chapter 5 suggests that the coevolutionary ratchet be-tween virus and immune system can be generalized to phenotype-phenotypeinteractions. That is, to the competition between the virus and the cognitiveimmune system. At the level of the pathogen-host system, the possible co-evolutionary stable states are either a highly variable phenotype-phenotypeconflict near a critical point, or else a fixed, phenotype-phenotype quasi-equilibrium point at the low variability end of the ratchet.

This dichotomy appears to be extended to structurally more complexpathogens, for example, malaria, which, although it is not near some evo-lutionary error catastrophe, has apparently nonetheless been ratcheted downto the high variability equilibrium point for phenotype coevolution.

The cognitive nature of the immune system may play an important rolehere. SIV, the simian version of HIV, in long-evolved relations with a host


species, exists at high blood titre without eliciting an inflammatory response(Gordon et al., 2005). In terms of the cognitive model of section (1.2), SIVantigen has been relegated to the ‘B0’ model of ‘not recognized’ rather thanthe ‘B1’ mode of immune attack. One speculates as to the possible impor-tance of cognitive gene expression in determining more complex phenotypiccoevolutionary processes. An example is perhaps found in the recent work ofLey et al. (2008) on the evolution of mammals and their gut microbes. Theyconclude that the tolerance of the immune system to gut microbes is a basaltrait in mammal evolution.

As stated at the end of chapter 5, however, a large deviations argumentsuggests that external mesoscale ecosystem shifts might well drive a relativelystable host-pathogen relationship from low to high variability, not a goodthing.

6.1.6 Implications of the model

Scientific enterprise encompasses the interaction of facts, tools, and theories,all embedded in a path-dependent political economy that seems as natural tous as air to a bird. Molecular biology, Central Limit Theorem statistics, and19th century mathematics, presently provide the reductionist tool kit mostpopular in the study of immune function and disease process. Many essentialmatters related to the encompassing social, economic, and cultural matrix sofundamental to human biology are simply blindsided, and one is reminded,not very originally, of the joke about the drunk looking for his missing carkeys under a street lamp, “because the light here is better.”

The asymptotic limit theorems of probability beyond the Central LimitTheorem, in concert with related formalism adapted from statistical physics,would seem to provide new tools. We think these can generate theoreticalspeculations of value in obtaining and interpreting empirical results aboutinfection and immune process.

Our model explicitly invokes the possibility of synergistic interaction be-tween the selection pressure of the immunocultural condensation (ICC) thatcharacterizes human immune response and the variable antigenic coat of anestablished pathogen population, particularly in the context of embeddingpatterns of structured psychosocial stress which, to take a Rate Distortionperspective, can literally write an image of itself onto that interaction. TheICC, through immune hypermutation and the choice of immune response pur-sued, may engage in its own second order selection. What results are first,second, and possibly mixed, order interpenetrations, in which the ICC andpathogens constitute each other’s selection pressure and selected structure,an interaction that may become a distorted image of enfolding patterns ofsocioeconomically, historically, and politically determined psychosocial stress.As the evolutionary anthropologist Robert Boyd put succinctly, Culture is asmuch a part of human biology as the enamel on our teeth (Boyd and Richerson


1995; Richerson and Boyd, 2004). It follows that any efforts to characterizeand respond to threats to human biology need account for culture’s roles.

Human chronic infection cannot, in particular, be simply abstracted asa matter of conflict between the pathogen and the immune system alone.Indeed, the concept of an immune system ‘alone’ has no meaning within ourmodel, in stark contrast with, for example, the well-stirred Erlenmeyer flaskpredator-prey population dynamics of Nowak and May (2000). The cells ofthe immune system comprise only the point of a long biocultural sword aimedat the throats of most infections.

Individual and collective history, socioeconomic structure, psychosocialstress and the resulting emotional states, may not be mere adjuncts to whatis termed basic science in the medical journals. Rather, they may be as mucha part of basic human biology as T-cells. Magic bullet vaccines, therapeuticdrugs, or highly-focused medicalized social interventions against HIV diseaseand other mutagenic parasites – approaches that inherently cannot reckonwith socioeconomic, historical, and cultural determinants of health and illness– will likely largely fail as they are overwhelmed by a combination of relentlesspathogen adaptation, cross-population variation in immune cognition, and aglobalized travel network that increasingly confronts host populations withmyriad pathogen variants. For chronic infections like HIV and malaria, in-dividual level or limited social network intervention strategies which neglectlarger embedding context, and the history of that context, embody a grosslyunreal paradigm of basic human biology.

We know that some social systems have succeeded in controlling malariathrough, for example, persistent and highly organized programs of insect vec-tor control. For HIV, humans are both vector and host. The larger socialcontext, then, plays a fundamental role in the individual- and population-level decisions that promote or decelerate the HIV epidemic (D. Wallace andR. Wallace 1998; Schoepf et al. 2000). The biological consequences of ignoringthe larger context are devastating, above and beyond the awful human costof the epidemic.

R.G. Wallace (2004) suggests that, alone, individual-level antiretroviraltreatment of the HIV epidemic may constitute a selection pressure forcingevolutionary changes in HIV life history, including, in one albeit remote pos-sibility, a more rapid onset of AIDS. A key result, however, is that increasinginfection survivorship and decreasing the transition rate from the asymp-tomatic stage to AIDS, as drug regimens aim to do, may induce the great-est increase in infection population growth. Because infection survivorship isphysiologically enmeshed with host survivorship the asymptomatic stage be-comes under the drug regimens a demographic shield against epidemiologicalintervention. In other words, HIV may use processes at one level of bioculturalorganization to defend itself against cures directed at it at other levels. Anysuccessful intervention, then, must display a comparable multidimensionality.

Cartesian reductionism internalizes causality by assuming the whole of anyphenomenon is a sum of its parts. Despite its successes, many (Wimsatt, 1980;


Bignami, 1982; Levins and Lewontin, 1985; Mayr, 1996; Levins, 1998; Oyamaet al., 2001; Van Regenmortel and Hull, 2002; Gould 2003) have pointed outthe problems with the reductionist approach in the study of biological phe-nomena, including of disease. Reductionism’s widespread application, even onproblems that do not yield to its approaches, is in part an outgrowth of socialdecisions about the role and nature of science.

Our work, here and cited, suggests a further complication. The conse-quences of reductionism’s failures do not merely include mischaracterizingepidemics. The nature of study itself can affect the evolution of pathogens. Thereductionist approach may very well, through a mesoscale resonance-drivenmicrobial ecosystem resilience domain shift, select for holistic or dialecticalresponses on the part of pathogens. Reductionism’s wholesale application,while succeeding against diseases such as polio and smallpox, welcome devel-opments notwithstanding, may select for diseases that are characterized bycomplex sociogeographies, multiple hosts, and multidimensional interactionsacross scale. The HIV, malaria, and tuberculosis epidemics, as we have dis-cussed, are obvious examples of holistic pathogens. In industrial countries,heart disease, cancer, and obesity take their toll; so-called diseases of afflu-ence the poorest and most marginalized typically suffer the worst (Wallace etal., 2003; Wallace, 2005a). The ecology literature tells us sources of mortalitycompete. While pharmaceuticals, surgery, and individual-level risk reductioninterventions control reductionist threats – additive sources of mortality bothwithin individuals and populations – the pathogenic playing field appears nowtilted towards holistic diseases we are largely unable to address because of therestricted scientific and medical practices pursued.

Our model raises the possibility of effective integrated pathogen manage-ment (IPM) programs through synergistic combinations of social, ecologi-cal, and medical interventions. IPM far transcends ‘medical’ strategies thatamount to little more than a kind of pesticide application, an approach in-creasingly abandoned in agriculture as simply inadequate to address pathogenevolutionary strategies.

Prospects for studying immunocultural condensation and implementing arelated IPM appear both exciting and difficult. New modes of interventionneed involve new means of modeling basic biology. While we can model theinteraction of first and second order phenomena in the context of structuredstress using network information theory, it is difficult to envision interactionbetween second order ‘tuning’ processes, or the mechanics of even higher or-der effects: can we continue to ‘tune the tuners’ in a kind of idiotypic hall ofmirrors? The mathematics would be straightforward, but the correspondingmolecular biology would have to be subtle indeed. Higher order interpenetra-tion – mutating the mutator – may be observable in certain isolated circum-stances, for example in the interplay between B-cell somatic hypermutationand a pathogen’s hypervariable membrane proteins. More likely some versionof rate distortion manifold retina-like focus operates. Clearly much work isneeded to trace the connections among the culture-specific and cognitive na-

6.2 Culture and the infection phenotype: case histories 121

ture of the immune system, pathogen adaptation, the information dynamicsof their interaction, the molecular manifestations of those dynamics, and theparticularities of intervention.

As a first effort toward testing the proposed relations among the ICC anddisease, we next qualitatively apply our paradigm to characterizing specificpathogens and the socioecological contexts in which they evolve.

6.2 Culture and the infection phenotype: case histories

6.2.1 Introduction

Following closely Wallace and Wallace (2002), we begin with a reconsiderationof some implications of the Atlan-Cohen perspective on immune cognition(Cohen, 1992, 2000; Atlan and Cohen, 1998) for understanding the role ofculture in the phenotypic expression of infectious disease, and the implicationsfor vaccine strategies when simple elicitation of sterilizing immunity fails.This will provide an introduction to more complicated circumstances in whichculture, and the policies which derive organically from it, can actually drivepathogen evolution.

The Atlan-Cohen view takes on special importance in the context of re-cent work by Nisbett et al. (2001) showing clearly that cognition in the centralnervous system (CNS) is not universal, but rather differs fundamentally forpopulations with different cultural systems. We propose the immune systemtoo may be a culture-specific condensation of sociocultural and biological cog-nition, in the same sense that neuroimmunology and immunogenetics describethe condensation of CNS and genetic ‘languages’ with immune function. Mod-ifying Boyd’s aphorism about culture described previously, we propose thatculture is as much a part of the human immune system as T-cells. It followsthat successful vaccine strategies where the smallpox model fails most likelymust take such immunocultural condensation into account. In this introduc-tory section we reinterpret recent studies of West African cultural variation inimmune response to malaria, and in the efficacy of interventions against it. Wealso review similar US cultural variation in HIV transmission. The approachneither reifies ‘race’ nor, as in much of the biomedical literature, denies theburdens of social and political histories.

Malaria and HIV are major causes of morbidity and mortality for whichno vaccine strategy has produced sterilizing immunity. Malaria has a compli-cated parasite life cycle with multiple and often changing antigens, and HIVis an evolution machine. Indeed, many, if not most, infectious diseases andmalignancies have basic ecological and life-cycle factors that obviate simpleeffective vaccination on the smallpox model.

Such complications are increasingly under scrutiny. For example interac-tions between the central nervous system (CNS) and the immune system, andbetween the genetic heritage and the immune system have become officially


recognized and academically codified through journals with titles such as Neu-roimmunology and Immunogenetics. Another complication, described in theprevious section, recognizes that the culture in which humans are socially em-bedded also interacts with individual immune systems to form a compositeentity that might well be labeled an immunocultural condensation, (ICC).

In the light of the ICC we reinterpret recent observations of culturally-specific immune response to malaria in West Africa, and to heterosexual AIDSin the US.

6.2.2 Genes, cognition, and culture

Increasingly, biologists excoriate simple genetic reductionism which neglectsthe role of environment. Lewontin (2000), for example, explains that genomesare not ‘blueprints,’ as genes do not ‘encode’ for phenotypes. Organisms areinstead outgrowths of fluid, conditional interactions between genes and theirenvironments, as well as developmental ‘noise.’ Organisms, in turn, shape theirenvironments, generating what Lewontin terms a triple helix of cause and ef-fect. Such interpenetration of causal factors may be embodied by an arrayof organismal phenomena, including, as we shall discuss, a fourth branch tothe Lewontin helix, that is, culture’s relationships with the brain, the immunesystem, and the ecology of infectious disease. We propose reinterpreting im-mune function in this light, with profound implications for medical and publichealth interventions for infectious diseases where the smallpox model fails.

The current vision of human biology among evolutionary anthropologistsis consistent with Lewontin’s analysis and is summarized by Durham (1991).Durham argues that genes and culture are two distinct but interacting sys-tems of inheritance within human populations. Information of both kinds hasinfluence, actual or potential, over behaviors which creates a real and un-ambiguous symmetry between genes and phenotypes on the one hand, andculture and phenotypes on the other. Genes and culture are best representedas two parallel lines or ‘tracks’ of hereditary influence on phenotypes.

A goodly part of hominid evolution can be characterized as an interweavingof genetic and cultural systems. Genes came to encode increasing hypersocial-ity, learning, and language skills. The most successful populations displayedincreasingly complex structures that better aided in buffering the local envi-ronment (Bonner, 1980). Every successful human population seems to have acore of tool usage, sophisticated language, oral tradition, mythology and mu-sic, focused on relatively small family/extended family groupings of variousforms. More complex social structures are build on the periphery of this basicgenetic-cultural object (Richerson and Boyd, 2004).

At the level of the individual, the genetic-cultural object appears to bemediated by what evolutionary psychologists postulate are cognitive moduleswithin the human mind (Barkow et al., 1992). At the risk of reifying a prefor-mationist ontology, each module was shaped by natural selection in responseto specific environmental and social conundrums Pleistocene hunter-gatherers


faced. One set of such domain-specific cognitive adaptations addresses prob-lems of social interchange (Cosmides and Tooby, 1992). Regardless of the exactorigins of the human mind, the human species’ very identity may rest, in part,on its unique evolved capacities for social mediation and cultural transmission.

The brain-and-culture condensation has been adopted as a kind of neworthodoxy in recent studies of human cognition. For example Nisbett et al.(2001) review an extensive literature on empirical studies of basic cognitive dif-ferences between individuals raised in what they call ‘East Asian’ and ‘West-ern’ cultural heritages. They view Western-based pattern cognition as ‘ana-lytic’ and East-Asian as ‘holistic.’ Nisbett et al. (2001) find that

[1]. Social organization directs attention to some aspects of the perceptualfield at the expense of others.

[2]. What is attended to influences metaphysics.[3]. Metaphysics guides tacit epistemology, that is, beliefs about the nature

of the world and causality.[4]. Epistemology dictates the development and application of some cog-

nitive processes at the expense of others.[5]. Social organization can directly affect the plausibility of metaphysical

assumptions, such as whether causality should be regarded as residing in thefield vs. in the object.

[6]. Social organization and social practices can directly influence the de-velopment and use of cognitive processes such as dialectical vs. logical ones.

Nisbett et al. (2001) conclude that tools of thought embody a culture’sintellectual history, that tools have theories build into them, and that usersaccept these theories, albeit unknowingly, when they use these tools.

We argue that the condensation between culture and both the gene andthe brain described here may also be found for the immune system. Nextwe briefly review some implications of the Atlan-Cohen arguments regardingimmune cognition.

6.2.3 Immune cognition and culture

Section 1.2.1 examined the Atlan/Cohen view of immune cognition at somelength. As we have shown earlier, it is possible to give Atlan and Cohen’slanguage metaphor of meaning-from-response a precise information-theoreticcharacterization, and to place that characterization within a context of recentdevelopments which propose the coevolutionary mutual entrainment of differ-ent information sources to create larger metalanguages with the originals assubdialects. This work, a formalism based on the Large Deviations Programof applied probability, permits treating gene-culture and brain-culture con-densations using a unified conceptual framework of information source coevo-lutionary condensation. Cohen’s immune cognition model suggests, then, thepossibility that human culture and the human immune system may be jointlyconvoluted. That is, there would appear to be, in the sense of the gene-cultureand brain-culture condensations of the previous section, an immune-culture


condensation as well. To neuroimmunology and immunogenetics we add ‘im-munocultural condensation’.

The evolutionary anthropologists’ vision of the world implies language,culture, gene pool, and individual CNS and immune cognition are intrinsicallymelded and synergistic. We propose that where the smallpox vaccine modelfails, culture and immune cognition may become a joint entity, determining,in considerable measure, the kind of vaccine strategy which may be effective.This effect may be confounded – and even masked – by the distinct populationgenetics often associated with linguistic and cultural isolation.

Africa contains great cultural and genetic diversity, suggesting the needfor severe local refining and monitoring of any vaccine strategy. Traditional‘case-control’ studies can, in fact, be profoundly compromised by linguisticand cultural differences which are convoluted with an associated genetic di-vergence that may be a simple marker of such difference rather than its cause.Similarly, the US, as a nation of immigrants, encompasses considerable cul-tural and genetic diversity, even in the context of both de-jure and de-factodeculturation.

In sum, population differences of immune function heretofore attributedto genetic factors alone may, rather, represent differences in immune cognitiondriven by, or, through the proposed ICC, synergistic with, profound culturaldifferences.

We reinterpret recent observations on malaria in Burkina Faso and het-erosexual AIDS in New Jersey from this perspective.

6.2.4 Malaria and the Fulani

Modiano et al. (1996, 1998, 2001) have conducted comparative surveys onthree roughly co-resident West African ethnic groups – which they describeas ‘sympatric’ – exposed to the same strains of malaria. The Fulani, Mossi,and Rimaibe live in the same conditions of hyperendemic transmission in aSudan savanna area northeast of Ouagadougou, Burkina Faso. The Mossi andRimaibe are Sudanese Negroid populations with a long tradition of seden-tary farming, while the Fulani are nomadic pastoralists, partly settled andcharacterized by non-Negroid features of possible Caucasoid origin.

Parasitological, clinical, and immunological investigations showed consis-tent interethnic differences in P. falciparum infection rates, malaria morbidity,and prevalence and levels of antibodies to various P. falciparum antigens. Thedata point to a remarkably similar response to malaria in the Mossi and Ri-maibe, while the Fulani are clearly less parasitized, less affected by the disease,and more responsive to all antigens tested. No difference in the use of malariaprotective measures was demonstrated that could account for these findings.Known genetic factors of resistance to malaria showed markedly lower fre-quencies in the Fulani (Modiano et al., 2001). The differences in the immuneresponse were not explained by the entomological observations, which indi-cated substantially uniform exposure to infective bites.


Modiano et al. (1996) conclude that sociocultural factors do not seem tobe involved, and that the available data support the existence of unknowngenetic factors, possibly related to humoral immune responses, determininginterethnic differences in the susceptibility to malaria.

In spite of later finding the Fulani in their study region have significantlyreduced frequencies of the classic malaria-resistance genes compared to theother ‘sympatric’ ethnic groups, Modiano et al. (2001) again conclude thattheir evidence supports the existence in the Fulani of unknown genetic fac-tor(s) of resistance to malaria.

This vision of the world carries consequences, seriously constraining in-terpretation of the efficacy of interventions. Modiano et al. (1998) conductedan experiment in their Burkina Faso study zone involving the distributionof permethrin-impregnated curtains (PIC) to the three populations, withmarkedly different results:

“ The PIC were distributed in June 1996 and their impact onmalaria infection was evaluated in [the three] groups whose baselinelevels of immunity to malaria differed because of their age and ethnicgroup. Age- and ethnic-dependent efficacy of the PIC was observed.Among Mossi and Rimaibe, the impact (parasite rate reduction afterPIC installation with respect to the pre-intervention surveys) was 18.8% and 18.5 %, respectively. A more than two-fold general impact (42.8%) was recorded in the Fulani. The impact of the intervention oninfection rates appears positively correlated with the levels of anti-malaria immunity...”

Most critically, Modiano et al. (1998) conclude from this experiment thatthe expected complementary role of a hypothetical vaccine is stressed by theseresults, which also emphasize the importance of the genetic background of thepopulation in the evaluation and application of malaria control strategies.

While we fully agree with the importance of the results for a hypotheticalvaccine, much in the spirit of Lewontin (2000) we beg to differ with the adhoc presumptions of genetic causality, which paper over alternatives involvingenvironment and development consistent with these observations.

The medical anthropologist Andrew Gordon has published a remarkablestudy of Fulani cultural identity and illness (Gordon, 2000):

“Cultural identity – who the Fulani think they are – informs think-ing on illnesses they suffer. Conversely, illness, so very prevalent in sub-Saharan Africa, provides Fulani with a consistent reminder of theirdistinctive condition... How they approach being ill also tells Fulaniabout themselves. The manner in which Fulani think they are sick ex-presses their sense of difference from other ethnic groups. Schemas of[individual] illness and of collective identity draw deeply from the samewell and web of thoughts... As individuals disclose or conceal illness, asthey discuss illness and the problem of others, they reflect standards


of Fulani life – being strong of character not necessarily of body, beingdisciplined, rigorously Moslem, and leaders among lessors... to be instep with others and with cultural norms is to have pride in the selfand the foundations of Fulani life.”

The Fulani carried the Islamic invasion of Africa into the sub-Sahara, en-slaving and deculturing a number of ethnic groups, and replacing the nativelanguages with their own. This is much the way African Americans were en-slaved, decultured, and taught English.

As Gordon puts it,

“ ‘True Fulani’ see themselves as distinguished by their aristocraticdescent, religious commitments, and personal qualities that clearlydiffer from lowland cultivators. Those in the lowland are, historically,Fulani subjects who came to act like and speak Fulani, but they arethought to be without the right genealogical descent. The separationbetween pastoralists and agriculturists repeats itself in settlementsacross Africa. The terms vary from place to place in Guinea, theterms are Fulbhe for the nobles and the agriculturalist Bhalebhe orMaatyubhee; in Burkina Faso, Fulbhe and the agricultural Rimaybhe;and in Nigeria, the Red Fulani and the agricultural Black Fulani... Theschemas for the Fulani body describe the differences between them andothers. These are differences that justify pride in being Fulani andnot Bhalebhe, Maatyubhe, Rimaybhe, or Black Fulani. In Guinea, theword ‘Bhalebhe’ means ‘the black one’. The term ‘Bhalebhe’ carriesthe same meaning as ‘Negro’ did for Africans brought to North Amer-ica. It effaces any tribal identity...

The control a Fulani exercises over the body is an essential featureof ‘the Fulani way.’ Being out of control is shameful and not at allFulani-like... To act without restraint is to be what is traditionallythought of as Bhalebhe...

Being afflicted with malaria – and handling it well – is a significantproof of ethnicity. How Fulani handle malaria may be telling. Whatthey lack in physical resistance to disease they make up in persistence.Though sickly, Fulani men only reluctantly give into malaria and forgowork. To give into physical discomfort is not dimo. When malaria issevere for a man he is likely not to succumb to bed, but instead to sitoutside of his home socializing.”

Parenthetically, many primate studies (e.g., Schapiro et al., 1998) showthat dominance rank, an important psychosocial factor, strongly and posi-tively affects immune response in a stable social setting, while a vast body ofparasitological observation and theory (e.g., Crofton, 1971) shows the ‘overdis-persion’ of parasites within affected populations – i.e., relative concentration– is closely but inversely related to social dominance.


Our Occam’s Razor hypothesis, then, is that the observed significant dif-ference in both malarial parasitization and the efficacy of intervention betweenthe dominant Fulani and co-resident ethnic groups in the Ouagadougou re-gion of Burkina Faso is largely accounted for by factors of immunoculturalcondensation, particularly in view of the lower frequencies of classic malaria-resistance genes found in the Fulani.

Given their protective ICC, the Fulani simply may not need those classicgenes.

It is not that the Fulani are not parasitized, or that the ‘Fulani way’prevents disease, but that the population-level burdens of environment aremodulated by historical development, and these are profoundly different forthe (former) masters and the (former) slaves.

6.2.5 ‘Heterosexual AIDS’ in Northern New Jersey

Studies by Skurnick et al. (1998) and Rohowsky-Kochan et al. (1998), un-der the general rubric of the Heterosexual Transmission Study (HATS), haveexamined 224 heterosexual couples discordant for HIV type 1 infection (onepartner HIV infected) and for 78 HIV-concordant couples (both partners HIV-infected) to identify demographic and behavioral risk factors for HIV trans-mission. A large subset of this cohort was subsequently studied for differencesin major histocompatibility complex (MHC)-encoded class I and class II anti-gens.

Couples were characterized by ‘ethnicity’ as ‘ Black, Non-Hispanic’, ‘White,non-Hispanic’, and ‘Hispanic’.

Skurnick et al. (1998) state

“In New Jersey, heterosexual transmission has played nearly aslarge a role in the AIDS epidemic as has injection drug use. Hetero-sexual contact was the category of transmission associated with thegreatest increase in reported AIDS cases from 1994 to 1995. The sever-ity of the epidemic and the frequency of heterosexual transmission innorthern New Jersey motivated us... to evaluate the importance of be-havioral and biological factors that facilitate or impede heterosexualtransmission of HIV...

Risk factors that had significant bivariate associations with con-cordance were included in a multiple logistic regression model to eval-uate their relative importance in their simultaneous effects on con-cordance... Ethnicity was the strongest correlate. Black and Hispaniccouples were both more likely to be concordant [in HIV infection] thanwere whites or others.”

This was no small effect. The odds ratio (OR) for concordance associ-ated with ‘Hispanic’ ethnicity was 4.9(1.9-12.7, P=0.001), that for ‘Black’ awhopping 8.6(2.9-25.3, P=0.0001). The numbers in parenthesis are the 95%confidence limits and the associated P-value.


A principal conclusion of Skurnick et al. (1998) was that ethnicity mayrelate to genetic differences in susceptibility of the uninfected partner or in-fectiousness of the infected partner. That is, genetic factors entirely internalto the couples themselves primarily determine their concordant or discordantstatus.

The subsequent paper by Rohowsky-Kochan et al. (1998) examined thegenetic hypothesis in more detail:

“Our results suggest that there may be different HLA alleles in-volved in the susceptibility and/or resistance to HIV infection in in-dividuals of different ethnic backgrounds. It is possible that an as yetunidentified susceptibility/resistance genetic factor for HIV infectionmay be linked with different HLA alleles in different ethnic back-grounds...

The American Caucasians... are a very heterogeneous group com-prised of a mixture of [identifiable] ethnic subpopulations...

[S]ignificant HLA associations with HIV resistance/susceptibilitywere detected in both Black and Hispanic cohorts but not in Cau-casians... suggest[ing] that genetic factors may play a role in the find-ing of Skurnick et al. (1998) that Black and Hispanic heterosexualcouples have a greater risk for HIV-1 concordance than Caucasiancouples.”

Again, alternative explanations consistent with the results are left unex-plored in favor of a simplistic genetic reductionism.

European colonialism in the Americas parallels, in critical respects, thatof the Fulani in Sub-Saharan Africa. ‘Black’ populations now speak English,and ‘Hispanic’ populations Spanish, and these terms efface tribal identity.

Although White ethnics can usually trace their past to some Europeanhomeland, African-Americans – ‘Negroes’, ‘Blacks’ – many of whom are, af-ter two hundred years of sexual exploitation in slavery and under AmericanApartheid, more than a little ‘White’, usually cannot. Intermediate are theHispanics in the US, who are, in spite of Spanish colonialism, more recog-nizably diverse. In Northern New Jersey they include self-identified Cubans,Puerto Ricans, Mexicans, Garafuna, Aymara, etc. etc., many of whom travelregularly to the homeland.

Northern New Jersey is, however, according to many studies (Massey andDenton, 1993; Acevedo-Garcia, 2000), one of the most heavily segregated re-gions of the US. Newark, the largest city in Northern New Jersey, in termsof what Massey and Denton (1993) call statistical measures of Unevenness,Isolation, Clustering, Centralization and Concentration, is even more segre-gated than nearby New York City, one of the world’s most segregated cities.As Massey and Denton (1993) put it, comparing African-Americans and His-panics,


“No other group in the contemporary United States comes closeto this level of isolation within urban society. US Hispanics, for ex-ample, are also poor and disadvantaged; yet in no metropolitan areaare they hypersegregated. Indeed, Hispanics are never highly segre-gated on more than three [of our five study factors] simultaneously...Despite their immigrant origins, Spanish language, and high povertyrates, Hispanics are considerably more integrated in US society thanare blacks.”

Given these circumstances, and taking malaria in Burkina Faso as a tem-plate, it seems evident that effects of the ICC in the context of the US systemof Apartheid ensure that Caucasian couples would show fewer genetic mark-ers of HIV than others, and that Blacks would show greater susceptibility toHIV transmission than Hispanics, and Blacks and Hispanics together, greatersusceptibility than Caucasians.

6.2.6 Conclusions and speculations

At the individual level, as opposed to community scales of space, time andpopulation, these matters are fairly well understood. Recent work by Kiecolt-Glaser and Glaser (1996, 1998, 2000), for example, has examined the effectof chronic stress on the efficacy of influenza, hepatitis-B, and pneumococcalpneumonia vaccine among elderly caregivers of dementia patients, and amongmedical students.

They found, for influenza, that the caregivers showed a poorer antibody re-sponse following vaccination relative to control subjects, as assessed by ELISAand hemagglutination inhibition. Caregivers also had lower levels of in vivovirus-specific-induced interleukin 2 levels and interleukin 1β. The data demon-strate that down-regulation of the immune response to influenza virus vacci-nation is associated with a chronic stressor in the elderly.

Similar effects were found among the elderly caregivers for response topneumoccocal pneumonia vaccination, leading to the conclusion that chronicstress can inhibit the stability of the IgG antibody response to a bacterialvaccine.

Medical students who reported greater social support and lower anxietyand stress demonstrated a higher antibody response to HEP-B surface antigenat the end of the study period.

Glaser et al. (1998) conclude that the differences in antibody and T-cellresponses to HEP-B and influenza virus vaccinations provide a demonstrationof how stress may be able to alter both the cellular and humoral immuneresponses to vaccines and novel pathogens in both younger and older adults.

We reiterate that a vast body of animal model studies involving sociallystructured populations shows clear impacts of acute and chronic social andother stressors on immune competence (e.g., de Groot et al., 2001; Gryazeva


et al., 2001; Stefanski et al, 2001). Elenkov and Chrousos (1999) in particu-lar suggest that glucocorticoids and catecholamines, the end-products of thestress system at the individual level, might selectively suppress cellular immu-nity, Th1 phenotype, in favor of humoral response – again at the individuallevel.

We now suggest, however, that the essential role of culture in human bi-ology takes matters considerably beyond such individual-level stress models,and into realms for which, to paraphrase Robert Boyd’s aphorism, culture isas much a part of the human immune system as are T-cells. We have char-acterized the interaction between immune and sociocultural cognition as animmunocultural condensation, and use the concept to provide an Occam’s Ra-zor explanation of observed differences in patterns of malarial parasitizationand response to intervention among co-resident ethnic groups in a section ofBurkina Faso, and rates of heterosexual transmission of AIDS within differentethnic groups in Northern New Jersey.

The relation between the Fulani and the Rimaibe mirrors the relationbetween ‘White’ and ‘Black’ residents of the US. Thus we suspect that differ-ences of ICC may play a large role in the health disparities evident betweenthose groups, an effect which persists even in the face of adjustment for so-cioeconomic factors. This suggests the continuing burden of history – whatorganizational ecologists and evolutionary biologists have come to call pathdependence – written upon the individual level ICC.

AIDS is a disease of marginalization and poverty, spreading along thestructural flaws of a society like water through cracks in ice. Crossectionalmarginalization and deprivation are synergistic with longitudinal path depen-dent, historically driven, structures of ICC to define the ecology of the in-fection. This perspective, unlike current simplistic geneticism, does not reify‘race’, but rather focuses on the central roles of culture, environment and de-velopment in the production of the ‘quadruple helix’ generating susceptibilityto, and expression of, infection by pathogens. The analysis directly incorpo-rates path dependence in a natural manner, making explicit the often-enduringeffects of historical patterns of social, political, and economic exploitation. Itgoes well beyond cross-sectional socioeconomic status analyses.

To the degree that factors of ICC dominate a disease ecology, there is un-likely to be an effective, single, one-size-fits-all vaccine strategy. On the otherhand, a more flexible attack which makes appropriate use of ICC mechanismsmay enjoy a synergistic boost in effectiveness, at least among those who donot bear the burdens of history. For those who do bear the burdens, however,as the experiment with insecticide-treated curtains in Burkina Faso implies,circumstances may be difficult indeed.

Many of these matters should be directly testable, using immune systemadaptations of Nisbett’s (2001) experimental techniques.

In the next section, we add the effects of HIV’s spatial economy on thevirus’ holistic evolution – a sociogeographic mode of farming pathogens.

6.3 Multiple Drug Resistant HIV in New York 131

6.3 Multiple Drug Resistant HIV in New York

6.3.1 Introduction

Human immunodeficiency virus (HIV) displays the strongest positive selectionof any known organism. The virus, then, should be expected to successfullyadapt to selection pressures generated by antiretrovirals, other microbicides,and vaccines. HIV can respond not only by developing multiple drug resis-tance, but also by significant alterations in life history strategy – increasedvirulence. Effective control of such a pathogen requires sophisticated multifac-torial ecosystem intervention, including a return to traditional public healthapproaches aimed squarely at improving living and working conditions amongthe marginalized populations which are the keystones of pandemic infection.

Here we examine the likely impacts of a stunning counter strategy, thecoevolutionary farming of the virus by a systematic program of forced dis-placement affecting poor African-Americans living in New York City’s mostheavily infected neighborhoods. The particular context is that the city is boththe principal driving epicenter for the hierarchical spatial diffusion of emerg-ing infections in the US and its economic partners, and is a central focus ofHIV itself.

A conference held in 1993 by the Office of the High Commissioner forHuman Rights of the United Nations characterized forced displacement inthese terms (UNHCHR, 1993):

“The practice of forced displacement involves involuntary removalof persons from their homes or land, directly or indirectly attributableto the State... The causes of forced evictions are very diverse. Thepractice can be carried out in connection with development and infras-tructure projects... housing or land reclamation measures, prestigiousinternational events, unrestrained land or housing speculation, hous-ing renovation, urban redevelopment or city beautification initiatives,and mass relocation or resettlement programmes...

The practice of forced displacement shares many characteristicswith related phenomena such as population transfer, internal displace-ment of persons, forced removals during or as a result or object ofarmed conflict, ‘ethnic cleansing’, mass exodus, refugee movements,etc....”

Here we examine a decades-long process of forced displacement affectingAfrican-Americans in New York City, with a special focus on the Harlem sec-tion of the Borough of Manhattan. We study the possible impacts of continu-ing displacement policies on the emerging scourge of multiply-drug resistant,or other evolutionarily transformed variants, of HIV.

A well-known report by Freeman and McCord (1990) examined excessmortality in Harlem, finding that, at the time, men in Bangladesh had a higherprobability of survival after age 35 than men in Harlem. They noted, almost in


passing, that Harlem’s population had declined from 233,000 in 1960 to only122,000 by 1980, with most of the population loss concentrated in the groupliving in substandard housing, much of it abandoned or partially occupiedbuildings. In that period the death rate from homicide increased from 25.3 to90.8 per 100,000, with cirrhosis and homicide together accounting for some33% of Harlem’s excess deaths between 1979 and 1981. By 1990 AIDS becamethe most common cause of death for persons between 25 and 44 years of agein Harlem.

The policy-driven process inducing that depopulation has been describedin some detail elsewhere (Wallace, 1990; R. Wallace and D. Wallace, 1997c; D.Wallace and R. Wallace, 1998, 2003; D. Wallace, 2001, and references therein).Withdrawal of essential housing-related municipal services, including fire ex-tinguishment resources, from minority voting blocks in the 1970’s triggeredprocesses of large-scale contagious urban decay and forced migration involvinga devastating synergism of fire, housing abandonment, and pathology (Wal-lace, 1988). The process was described by the New York State Assembly Re-publican Task Force on Urban Fire Protection (Task Force, 1978) as follows:

“There is mounting evidence that the lack of fire protectionwhich has plagued communities in the South Bronx, Central Harlem,Brownsville and Bushwick is assuming city-wide dimensions as itspreads to [other neighborhoods]... there are indications the City Plan-ning Commission and other agencies condoned [fire service] reductionsin the context of a ‘planned shrinkage’ policy... there is strong evi-dence that these actions have resulted in unwarranted loss of life anddestruction of city neighborhoods...”

After examining the consequences Wallace (1990) wrote:

“...[T]he... origins of public health and public order are much thesame and deeply embedded in the security and stability of personal,domestic and community social networks and other institutions...[D]isruptions of such networks, from any cause, will express themselvesin exacerbation of a nexus of behavior, including violence, substanceabuse and general criminality. These in turn have the most severe im-plications for...[many pathologies including the] evolution and spreadof AIDS.”

The policy-driven displacement of population affecting Harlem between1970 and 1980 created a massive de-facto refugee camp environment for emerg-ing and re-emerging infection. By 1990 Harlem was an epicenter of both AIDSand tuberculosis, and of their interaction (D. Wallace and R. Wallace, 1998,2003; R. Wallace and D. Wallace, 1997a; D. Wallace, 2001).

By 2005 Harlem and East Harlem rivaled the Gay center of New YorkCity, Manhattan’s Chelsea-Clinton neighborhood, in rates of HIV diagnosesper 100,000 population, respectively 132.4, and 108.2, vs 135.0. Age-adjusted


death rates per 1000 persons with AIDS were, however, quite different: 31.9and 32.6 vs. 11.4 (NYCDOH, 2006). This divergence represents not only acontrast in the effective availability of antretroviral drugs, but also obviouspopulation differences in patterns of burden and affordance between African-Americans, other minorities, and middle-class Whites, in spite of similarlydraconian pressures enforcing the social and spatial segregation of ethnic andsexual minorities in the United States (R.G. Wallace, 2003; Massey and Den-ton, 1992).

The planned shrinkage program, which exacerbated the spread of AIDSand tuberculosis (Wallace and Wallace, 1998), had, by 1990, set the stage fora subsequent round of displacement. The loss of economic, social, and politicalcapital consequent on the induced contagious urban decay of the 1970’s leftHarlem without effective means of resisting ‘gentrification’ by majority pop-ulations, that is, the ongoing reduction of Harlem to a largely-White ‘CentralPark North’.

Newman and Wyly (2006) describe this as follows:

“Central Harlem received an influx of middle-class residents through-out the 1970s and 1980s but the changes during the late 1990s andearly 2000s are different. Harlem’s residents report a solid flow ofSUV’s (sports utility vehicles) of people driving through the neigh-borhood scouting for homes. One resident described the housing de-mand: ‘People are coming up while you’re on the street asking whoowns the building. It’s a daily thing’. The neighborhood also appealsto renters seeking livable space with manageable commutes. In lessthan 15 minutes, residents are whisked to midtown on a 2 or A train;in 30 minutes, they can reach jobs on Wall Street. A 20-minute cabride gets you to LaGuardia Airport and every highway intersects withHarlem. Rents for floor-through apartments in brownstones are cap-turing $1,700 a month.”

They conclude:

“According to neighborhood informants, many [of those displacedby the rise in rents] are moving out of the city to upstate New York,New Jersey and Long Island... Those who are forced to leave gentri-fying neighborhoods are torn from rich local social networks of infor-mation and cooperation (the ‘social capital’ much beloved by policy-makers); they are thrown into an ever more competitive housing mar-ket shaped by increasingly difficult trade-offs between affordability,overcrowding and commuting accessibility to jobs and services. Allof the pressures of gentrification are deeply enmeshed with broaderinequalities of class, race and ethnicity, and gender... As affordablehousing protections are dismantled in the current wave of neo-liberalpolicy-making, we are likely to see the end-game of gentrification asthe last remaining barriers to complete neighborhood transformation


are torn down... Low-income residents who manage to resist displace-ment may enjoy a few benefits from the changes brought by gentrifica-tion., but these bittersweet fruits are quickly rotting as the supportsfor low-income renters are steadily dismantled.”

The forced displacement of New York City’s African-American popula-tion to a suburban/exurban ring around New York City, much like the Blacktownships surrounding Capetown, can be expected to induce a new round ofrefugee camp behavioral syndromes which will further exacerbate the spreadof HIV among African-Americans. At present African-Americans account for15% of the US population, but constitute over half of new HIV infections.

Katrina-like dispersal of New York City’s communities of color can beexpected to fatally compromise:

[1] ongoing antiretroviral drug treatment of those already infected withHIV,

[2] the effectiveness of treating new cases with antiretrovirals, and[3] virtually all possible infection prevention strategies.This will, in all likelihood, markedly accelerate the development and spread

of drug resistant viral strains.Mathematical analysis of contagious process in a commuting field (Wal-

lace et al., 1997, 1999; Wallace, 1999) suggests that, for national hierarchicaldiffusion, Metropolitan Regions are the systems of fundamental interest. Fromthat perspective, a disease epicenter has much the same large-scale force ofinfection whether it is concentrated in the center, or dispersed around the pe-riphery, of a particular large city: urban-suburban linkages are strong enoughto create a functional equivalence (Wallace, 1997).

Given the powerful central role of New York City and its metropolitanregion in the economic and political function of the American Empire, as wehave come to know it, larger scale, that is, international, hierarchical diffu-sion of infection from it can be expected to occur. Recent elegant, and verydisturbing, phylogeographic analysis by Gilbert et al. (2007) clearly confirmsthat the first wave of international spread of HIV was driven by incubationwithin the United States. Their work demonstrates convincingly that, for HIV-1 group M subtype B, the predominant variant in most countries outside ofsub-Saharan Africa, while the virus had an initial transfer event from Africato Haiti around 1966, the key to subsequent geographic diffusion was whatthen happened in the United States:

“...[A]ll..subtype B infections from across the world emanated froma single founder event linked to Haiti. This most likely occurred whenthe ancestral pandemic clade virus crossed from the Haitian commu-nity in the United States to the non-Haitian population there.... HIV-1was circulating in one of the most medically sophisticated settings inthe world for more than a decade before AIDS was recognized... [Thatis],[o]ur results suggest that HIV-1 circulated cryptically in the Unitedstates for ≈ 12 years before the recognition of AIDS in 1981.”


The essential inference is not that ‘AIDS originated in Haiti’, but ratherthat HIV-1 group M subtype B became entrained into the US social andspatial system, strongly dominated by New York City and its metropolitanregion, where it circulated for over a decade, and then spread hierarchicallyfrom the US to its trading partners. This is the pattern which may be ex-pected for drug resistant or other evolutionarily transformed variants of thevirus which are now incubating in the vast marginalized subpopulations ofthe United States.

A recent comprehensive review by Jones et al. (2008), which examined thepattern of emerging infections from 1940 to 2004, not just AIDS, broadly con-firms this analysis. They found that two developed regions strongly dominatedthe expression of all new diseases in that period: the Northeast Corridor of theU.S, including Boston, New York, Philadelphia, Baltimore, and WashingtonD.C., each of which has a vast marginalized subpopulation, and the GreaterLondon metro region.

We recapitulate something of the evolutionary biology of HIV and of thecanonical pattern of hierarchical disease diffusion within the US, and end withthe implications of African-American forced displacement for both nationaland international spread of evolutionarily transformed HIV.

6.3.2 Evolutionary biology of HIV

Affluent populations in the US have, at least in the short term, benefitedgreatly from the introduction of highly active antiretroviral therapy (HAART)against HIV. From 1995 to 1997, for example, HIV/AIDS deaths declined 63%in New York City, primarily among middle-class, and highly organized, Gaymales (Chiasson et al., 1999). Declines in AIDS deaths have otherwise beenquite heterogeneous, depending critically on both the economic resources andcommunity stability of affected populations (e.g., R.G. Wallace, 2003).

At present, AIDS deaths in the US are, largely, another marker of long-standing patterns of racism and socioeconomic inequity (e.g., Wallace and Mc-Carthy, 2006; R. Wallace et al., 2007). Those who have economic resources, orreside in stable communities not subject to various forms of redlining and/orde-facto ethnic cleansing, have effective access to HAART. Others, withoutresources, do not have such access.

HIV is, as indeed are most retroviruses, however, an evolution machine(Rambaut et al., 2004) which, at the individual level, almost always developsmultiple drug resistance, resulting in overt AIDS and subsequent prematurefatality. Such response to chemical pesticides, as has been the case with myr-iad other biological pests, is now becoming manifest at the population level.By 2001, in the US some 50% of patients receiving antiretroviral therapy wereinfected with viruses that express resistance to at least one of the availableretroviral drugs, and transmission of drug-resistant strains is a growing con-cern (Clavel and Hance, 2004; Grant et al., 2002). Multiple drug resistant(MDR) HIV is, in fact, rapidly becoming the norm, and the virus may even


develop a far more virulent life history strategy in response to the evolution-ary challenges presented by HAART, its successor microbicide strategies, orplanned vaccines (R.G. Wallace, 2004; Wallace and Wallace, 2004), a circum-stance which may have already been observed (e.g., Simon et al., 2003).

The review by Rambaut et al. (2004) puts the matter thus:

“HIV shows stronger positive selection than any other organismstudied so far... [its viral] recombination rate... is one of the highestof all organisms... Within individual hosts, recombination interactswith selection and drift to produce complex population dynamics, andperhaps provide an efficient mechanism for the virus to escape fromthe accumulation of deleterious mutations or to jump between adap-tive peaks. Specifically, recombination might accelerate progression toAIDS and provide and effective mechanism (coupled with mutation)to evade drug therapy, vaccine treatment or immune pressure... Moreworryingly, there is evidence that some drug-resistant mutants showa greater infectivity, and in some cases a higher replication rate, com-pared with viruses without drug resistant mutations.”

R.G. Wallace (2004) finds that

“...HAART may select for... an HIV with a semelparous life his-tory and a precocious senescence... [which] may be embodied by anaccelerated time to AIDS or related pathogenesis... Because infectionsurvivorship is physiologically enmeshed with host survivorship theasymptomatic stage becomes under HAART a demographic shieldagainst epidemiological intervention. The results appear to exemplifyhow pathogens use processes at one level of biological organization todefend themselves against impediments directed at them at another.”

Above we have suggested that as population-level structured stress ap-pears a fundamental part of the biology of many chronic infectious diseasesincluding AIDS. This raises the possibility that simplistic individual-orientedmagic bullet drug treatments, vaccines, and risk-reduction programs that donot address the fundamental living and working conditions which underliedisease ecology will fail to control many current epidemics. In addition, suchreductionist interventions may go so far as to select for more holistic pathogenscharacterized by processes operating at multiple levels of biocultural organi-zation.

MDR-HIV is already emerging in the very epicenters and epicenter popu-lations where HIV itself first appeared (Clavel and Hance, 2004), since thesewere the first to benefit from HAART, and thus seems likely to follow diffu-sion patterns similar to those of the earlier stage of the AIDS epidemic. Moregeneral ET-HIV’s can be expected to follow a similar pattern. We reconsiderthe initial period.


6.3.3 Hierarchical diffusion

Infectious disease is often seen as a marker for underlying urban structure.For example, Gould and Tornqvist (1971, p. 160) write:

“As the urban lattice hardens, and the links between the majorcenters strengthen, the dominant process is apt to change from a [spa-tially] contagious to a hierarchical one.

We have few examples of this dramatic change in innovation dif-fusion, but one particularly striking one comes from the early historyof the United States (Pyle, 1969). The disease cholera is hardly aninnovation we would like to spread around, but it does form a use-ful geographical tracer in a spatial system, rather like a radioactiveisotope for many systems studied by the biological sciences. The firstgreat epidemic struck in 1832 at New York and Montreal, and thendiffused slowly along the river systems of the Ohio and Great Lakes.A graphical plot of the time the disease was first reported againstdistance shows a clear distance effect, indicating that basically pro-cesses of spatial contagion were operating. A plot of time against citysize shows no relationship whatsoever. However, by 1849, the rudi-mentary urban hierarchy of the United States was just beginning toemerge. The second epidemic struck at New York and New Orleansin the south, and a plot of first reporting times against city size, indi-cates that a hierarchical effect was beginning to structure innovationflows at this time. Finally, in 1865, when the third epidemic struck,the railways were already strengthening the structure of America’surban space. The disease jumped rapidly down the urban hierarchy,and a plot of reporting time against city size shows that a very clearhierarchical process was at work.”

The first stages of the AIDS pandemic in the US provide a modern ex-ample. The cover of Gould’s 1993 book The Slow Plague, with more detail inGould (1999), presents a time sequence of maps showing the number of AIDScases in the US on a logarithmic scale. Cases first appear in the largest USport cities: New York, Los Angeles, San Francisco, Miami and WashingtonDC. Subsequent spread is by hierarchical hopscotch to smaller urban centers,followed by a spatially contagious winestain-on-a-tablecloth diffusion from citycenter into the surrounding suburban counties.

Figure 6.1, from Wallace et al. (1999), gives a detailed analytic treatment ofthe hierarchical hopscotch. Using multivariate analysis of covariance, it showsthe log of the number of AIDS cases in each of the 25 largest US metropolitanregions for two periods, [1] through April, 1991 and [2] from April 1991 throughJune 1995, as functions of a composite index defined in terms of a region’slocal pattern of susceptibility and its position in the US urban hierarchy. Thelocal indices are (i) the log of the number of violent crimes in the region for1991, and (ii) an index of ‘rust belt’ deindustrialization, the log of the ratio


of manufacturing employment in 1987 to that in 1972. The global index, ofposition on the US urban hierarchy, is the log of the probability of contactwith the New York City metro region, the nation’s largest, determined from acounty-by-county analysis of migration carried out by the US Census for theperiod 1985-1990.

Fig. 6.1. Log number of AIDS cases in the 25 largest US metropolitan regions,through 4/91 and 4/91-6/95. The composite index is X = .764 Log(USVC91) + .827Log(USME87/USME72) + .299 Log(Prob. NY). USVC91 is the number of violentcrimes, USMEnm the number of manufacturing jobs in year nm, and (Prob. NY) theprobability of contact with New York City according to Census migration data for1985-1990. Applying multivariate analysis of covariance, the two lines are parallelwith different intercepts: The second is obtained simply by raising the first. The NewYork Metropolitan Region (NYMR) is at the upper right of the graph. The patternis consistent with the assumption that the NYMR drives the hierarchical diffusion ofHIV nationally. This suggests a powerful, coherent, national-scale, spatiotemporalhierarchical diffusion strongly linking marginalized communities in the NYMR, theApartheid policies which marginalize them, and the epidemic outbreak within them,to the rest of the country.

Locally, high levels of violence and industrial displacement represent bust-town and boom-town social dynamics leading to the loosening of social con-trol. Nationally, the probability of contact with New York represents inversesocio-spatial distance from the principal epicenter of the US AIDS epidemic.Multivariate analysis of covariance finds the lines for the two time periods


are parallel and each accounts for over 90 % of the variance in the dependentvariate. Thus later times are obtained from the earlier simply by raising thegraph in parallel. This means that processes within the New York Metropoli-tan Region, the upper right point of the graph, drive the national hierarchicaldiffusion of AIDS during this time span, the pre-HAART period of AIDSspread. We take this as representing a propagating, spatio-temporally co-herent epidemic process which has linked disparate, marginalized ‘core group’neighborhoods of Gay males, intravenous drug users, and ethnic minority pop-ulations across time and space with the rest of the urbanized US, ultimatelyplacing some 3/4 of the nation’s population at increasing risk: as go the NewYork Metropolitan Region’s segregated communities, so goes the Nation. SeeWallace, Wallace et. al (1999) for details, and Abler et al. (1971) or Gould(1993, 1999) for more general background.

The results of Gilbert et al. (2007) prove conclusively that a similar patternaffects the hierarchical spread of HIV variants from the US to its principaltrading partners. The US, and by inference its dominant conurbation, the NewYork Metropolitan Region, served as the primary source for diffusion of HIV-1 group M subtype B to the industrialized world, and will almost certainlycontinue to do so for its evolutionary transformed variants.

The social and geographic spread of infectious disease within a polity isconstrained by, and must be consistent with, an underlying sociogeographyin which segregated and oppressed subgroups traditionally constitute eco-logical keystone populations. Acutely marginalized communities within andsurrounding the largest cities are particularly central.

In contrast to the conclusions of Jones et al., (2008), who inferred a ‘mis-match’ in global resources currently allocated to emerging infectious diseasesurveillance and control, with developed countries receiving, in their view,an unneeded preponderance of resources, we see a two-fold, synergistic pro-cess affecting diffusion of HIV and other emerging infections, which may besummarized as:

[1] All roads lead to Rome.[2] All roads lead from Rome.That is, at first, de-facto colonial exploitation of economically peripheral

zones by the American Empire and its more developed client states, createscircumstances ripe for the emergence of new infectious disease by a variety ofmechanisms. These pathogens are then entrained by economically determinedtravel patterns into the largest urban centers of the US and its allies (inparticular the Northeast Corridor of the US, and the London Metro Region),which serve as the New Rome of the current imperial system.

Second, the domestic version of the US colonial enterprise, in particularthe fatal legacy of slavery, which developed into the present system of Amer-ican Apartheid (sensu Massey and Denton, 1992), has created vast marginal-ized populations within the nation’s largest metropolitan regions, particularlythe Northeast Corridor. Newly-imported emerging infections then incubatelargely unnoticed within these huge permanent de-facto refugee camps, and


subsequently blow back down the US urban hierarchy, and across to its moredeveloped client states, in particular the European Union.

There are several implications of this model for HIV. Most simply, thefind-the-cure ‘Treatment Culture’ which has dominated both official and non-governmental organizations’ AIDS policy in the US for some time, and partic-ularly since the development of HAART, is ending as HIV evolves resistanceto drug regimens or alters its life history (R.G. Wallace, 2004; Simon et al.,2003; Wallace and Wallace, 2004). Possible vaccines seem similarly challengedby HIV’s protean evolutionary nature, which allows the virus rapidly evolveout from under immune suppression. Indeed, a consensus is now emergingthat the twenty-year search for a vaccine against HIV has made no progress,with little hope for future results (Baltimore, 2008).

As the AIDS Treatment and Vaccine subcultures disintegrate under therelentless pressure of pathogen evolution new social organizations must emergeto confront the disease. Traditional public health approaches, which addressunderlying structural factors responsible for disease incubation and spread atthe population level – primarily the power relations between groups – havelargely been abandoned in the US for reasons of political expediency. Thefield is now dominated by a kind of neo-liberal, rightist intellectual analog tothe Stalinist sophistry of the fallen Soviet Union, effectively a Center-RightLysenkoism strongly driven by funding biases.

Controlling MDR, vaccine-resistant and other ET-HIV’s will require res-urrection of traditional public health, but this will be difficult because, in theUS, so much of the discipline’s history has been lost in favor of the blame-the-victim, medicalized, and individual-oriented perspectives now popular withthe current crop of major AIDS funding agencies and their client organiza-tions. Many resulting projects are characterized as ‘fundable trivialities’ or‘planting a tree in a desert’ even by foundation staff administering financialsupport.

ET-HIV’s are now poised to spread from the main US AIDS epicenters,particularly the New York Metropolitan Region, following much the samepatterns as the pre-HAART pandemic. In contrast, evidence exists that, forat least one more egalitarian social system – Amsterdam – there is a decliningtrend in transmission of drug-resistant HIV (Bezemer et al., 2004).

What is also clear, at least in the New York Metropolitan Area whichdrives the hierarchical diffusion of all emerging infection (Gould, 1993, 1999),and thus a keystone in the international spread of HIV variants from the US toits trading partners (Gilbert et al., 2007; Jones, et al., 2008), is that rebuildingof housing lost to prior policies of ethnic cleansing and stabilizing remaininglow income housing, is necessary for both regional and national control ofET-HIV’s. The current gentrification of Central Harlem and other commu-nities of color, given the region’s recent history, will simply further tightenthe contact probability field which links metropolitan counties (e.g. Wallaceand McCarthy, 2007 and references therein), and thus hasten the diffusionof the new virus within the New York Metropolitan Region. As a result of

6.4 Avian influenza 141

its dominance and sociogeographic centrality in humanity’s ecosystem, NewYork HIV will be catapulted throughout the United States and the rest of theworld.

In sum, displacing African-American and other poor populations fromHarlem and East Harlem into the lower-rent suburban periphery will cre-ate refugee camp conditions in the outlying New York Metropolitan Regionfor the development and international spread of evolutionarily-transformedHIVs, including multiple-drug-resistant strains of the virus. Urban-suburbanlinkages are strong in and near New York City, and can be expected to linkperiphery and center in a new, virulent ecology of ET-HIV which will thendiffuse down the urban hierarchy, then from city center to suburban ring,effectively placing at increased risk some 3/4 of the US population. Subse-quent spread of ET-HIV’s to other industrialized countries will likely followthe pattern uncovered by Gilbert et al. (2007).

At present, with condominiums presently selling for an average of well overUS $1.2 million each in Manhattan, assembling a package of only a dozen orso 100 unit apartment houses in Harlem represents a potential profit of nearlyUS $1 billion. For a billion dollars most developers, and their clients amongpublic officials and the leaders of non-governmental organizations, are unlikelyto give much thought to the national and international diffusion of multiple-drug-resistant HIV. Pushing poor people out offers too much opportunity forprofit. The results seem likely to establish the New York Metropolitan Regionas the global source of MDR-HIV in much the same manner that China’sGuangdong Province has, for deep structural reasons, become the epicenterfor worldwide transmission of highly pathogenic influenza A H5N1. the avianinfluenza virus.

6.4 Avian influenza

6.4.1 Panic in the city

Hong Kong, March 1997. An outbreak of deadly avian influenza sweepsthrough poultry on two farms (Davis, 2005; Greger, 2006). The outbreaksubsides, but two months later a three-year-old boy dies of the same strain,identified as a highly pathogenic version of influenza A (H5N1). Officials areshocked. This appears the first time such a strain has jumped the species bar-rier and infected a human. Shocking too, the outbreak proves persistent. InNovember a six-year-old is infected, recovering. Two weeks later, a teenagerand two adults are infected. Two of the three die. Fourteen additional infec-tions rapidly follow.

The deaths spur panic in the city and, with the onset of the regular flu sea-son, send many patients to the hospital worried their symptoms might be thoseof the new flu. By mid-December poultry begin to die in droves in the city’smarkets and it now seems most humans infected had handled birds. Hong


Kong acts decisively on that information. Authorities order the destructionof all of Hong Kong’s 1.5 million poultry and block new imports from Guang-dong, the mainland province across the Shenzhen River from which some ofthe infected birds had been transported. Despite another human death inJanuary, the outbreak is broken.

The poultry infected with this version of the virus suffer more than thegastrointestinal condition typical of avian influenza. The clinical manifesta-tions include swelling of the wattles and infraorbital sinuses, congestion andblood spots on the skin of the hocks and shanks, and a blue discolorationof the comb and legs (Yuen and Wong, 2005). The latter is characteristic ofthe cyanosis and oxygen deprivation suffered by many human victims of the1918 pandemic. Internally, infected poultry are marked by lesions and hemor-rhaging in the intestinal tract and the trachea, with blood discharge from thebeak and cloaca. Many birds also suffer infection in other organs, includingthe liver, spleen, kidney, and the brain, the last infection leading to ataxiaand convulsion.

Most worrisome for human health is this strain’s capacity for broadxenospecific transmission. The Hong Kong outbreak, first alerting the world toH5N1, infected humans with an influenza much more pathogenic than the rela-tively mild infections of other avian outbreaks that have intermittently crossedover into human populations. These patients presented with high fever, laterdeveloping some combination of acute pneumonia, influenza-like illness, upperrespiratory infections, conjunctivitis, pharyngitis, and a gastrointestinal syn-drome that included diarrhea, vomiting, vomiting blood, and intestinal pain(Bridges et al., 2000; de Jong et al. 2006). Patients also suffered multiple-organdysfunction, including that of the liver, kidney, and bone marrow. The respira-tory attacks involved extensive infiltration of both lungs, diffuse consolidationof multiple infected loci, and lung collapse.

If much of H5N1’s morbidity is distressing, its associated mortality isalarming. Once infected, the lungs’ vasculature becomes porous and fibrinogen-a protein involved in blood clotting-leaks into the lungs (de Jong et al., 2006).The resulting fibroblast exudates clog the lungs’ alveolar sacs, where gas ex-change takes place, and an acute respiratory disease syndrome results. In adesperate effort to save its charge, the immune system recruits such a stormof cytokines that the lungs suffer oedema. In effect, patients drown in theirown fluid only days after infection.

After Hong Kong, H5N1 slipped somewhat underground with local out-breaks largely limited to birds in southern China. During this time the virusunderwent the first of a series of reassortment events, in which several ge-nomic segments were replaced with those from other serotypes, reemergingas a human infection in Hong Kong in 2002 (Li et al., 2004; Webster et al.,2006). The following year H5N1 again reemerged, this time with a vengeance.The Z genotype that surfaced as the dominant recombinant spread acrossChina, into Vietnam, Thailand, Indonesia, Cambodia, Laos, Korea, Japan,and Malaysia. Two additional strains would subsequently materialize. Since


2005 the Qinghai-like strain has spread across Eurasia, as far west as England,and into Africa (Salzberg et al. 2007). The Fujian-like strain, emerging from itseponymous southern China province, has spread regionally across SoutheastAsia and, more recently, into Korea and Japan (Smith et al., 2006).

Since 2003 H5N1 has infected 387 humans, killing 245 (WHO, September,2008). Most of these infections have been poultry related; often the children ofsmall farmers playing with a favorite bird. But an increasing number of doc-umented cases of human-to-human transmission have accumulated-in HongKong, Thailand, Vietnam, Indonesia, Egypt, China, Turkey, Iraq, India, andPakistan (Kandan et al., 2006; Yang et al., 2007). The short chains of trans-mission have largely consisted of relatives living with or tending a patient. Theworry, well publicized, is that H5N1 will improve upon these first infections,evolving a human-to-human phenotype that ignites a worldwide pandemic.

The geographic diffusion of the virus is intimately related to the emergenceof such a phenotype. As are other pathogens, H5N1 is finding the regions ofthe world where animal health surveillance remains underdeveloped or de-graded by national structural adjustment programs associated with interna-tional loans (Rweyemamu et al., 2000). There is now too a greater integrationof aquaculture and horticulture, a burgeoning live-bird market system, andwidespread proximity to backyard fowl (Gilbert et al., 2007; Cristalli andCapua, 2007). Rural landscapes of many of the poorest countries are nowcharacterized by unregulated agribusiness pressed against periurban slums(Guldin, 1993; Fasina et al., 2007). Unchecked transmission in vulnerableareas increases the genetic variation with which H5N1 can evolve human-specific characteristics. In spreading over three continents fast-evolving H5N1also contacts an increasing variety of socioecological environments, includinglocale-specific combinations of prevalent host types, modes of poultry farming,and animal health measures.

In this way, by a type of escalating demic selection, H5N1 can betterexplore its evolutionary options (Wallace and Wallace, 2003). A series of fitvariants, each more transmissible than the next, can evolve in response tolocal conditions and subsequently spread. The Z reassortant, the Qinghai-likestrain, and the Fujian-like strain all outcompeted other local H5N1 strainsto emerge to regional and, for the Qinghai-like strain, continental dominance.The more genetic and phenotypic variation produced across geographic space,the more compressed the time until a human infection evolves.

6.4.2 Farming deadly influenza

Despite its impacts epidemiological and psychological, Hong Kong’s H5N1represented no first outbreak of avian influenza. In fact, within the UnitedStates alone, where the southern Chinese H5N1 has yet to reach, there havebeen a series of outbreaks the past decade. These outbreaks were typically lowpathogenic, causing lesser damage to poultry. There was, however, an outbreakof highly pathogenic H5N2 in Texas in 2002. A low pathogenic H5N2 outbreak


in California, beginning in farms outside of San Diego, evolved greater viru-lence as it spread through California’s Central Valley (Davis, 2005). Anotheroutbreak worthy of note is that of a low pathogenic strain of H5N1 in Michiganin 2002. H5N1, then, has already invaded the United States in a less deadlyform, telling us that the molecular identity of a strain is insufficient for defin-ing the danger of any single outbreak. Low and high pathogenic strains mustbe distinguished otherwise. Some mechanism must transform low pathogenicstrains into more virulent ones (and, we should hope, back again).

The nastiness of the southern Chinese H5N1 may be in part due to anantigenic shift to which we presently have no immunity. Humans have thispast century been infected almost exclusively by H1, H2, and H3 strains towhich we have developed antibody memory. When many of us are confrontedby another strain of these same types we can slow down the infection. We havepartial immunity at the individual level and herd immunity at the populationlevel. Since we have never been exposed to H5 infections en masse we havenothing to slow down infection within each person and nothing to keep itdamped down across the population. What cannot be slowed down arrivesearlier. It is likely then that, as was the case for the 1957 and 1968 pandemics,the main wave of the next new human-to-human influenza will sweep theplanet earlier than the typical seasonal flu, perhaps even as early as Augustsome terrible year in the near future (Cliff et al. 1986).

But how are we to account for an increase in virulence within a particularflu subtype? Recall the low pathogenic strain of H5N1 in Michigan. Anotherexplanation leans on a large modeling literature (reviewed by Dieckmann etal., 2002; Ebert and Bull, 2008) that hypothesizes a relationship between therate of transmission and the evolution of virulence, the amount of damagea strain causes its host. Simply put, to start, there is a cap on pathogenvirulence. Pathogens must avoid evolving the capacity to incur such damageto their hosts that they are unable to transmit themselves. If a pathogen killsits host before it infects the next host it destroys its own chain of transmission.But what happens when the pathogen ‘knows’ that the next host is comingalong much sooner? The pathogen can get away with being virulent becauseit can successfully infect the next susceptible in the chain before it kills itshost. The faster the transmission rate, the lower the cost of virulence.

A key to the evolution of virulence is the supply of susceptibles (Lipsitchand Nowak, 1995). As long as there are enough susceptibles to infect, a virulentphenotype can work as an evolutionary strategy. When the supply runs out itdoes not matter what virulence a pathogen has evolved. Time is no longer onthe particular strain’s side. A failed supply of susceptibles, drained by highmortality or rebound immunity, forces all influenza epidemics to ultimatelyburn out at some point. That’s cold comfort, of course, if millions of peopleare left dead in a pandemic’s wake.

What caused southern China’s H5N1 to evolve its breathtaking virulence?The circumstantial evidence points overwhelmingly to factory farming (Short-ridge, 2003; FAO, 2004; Greger 2006). Growing genetic monocultures removes


whatever immune firebreaks may be available to slow down transmission (Gar-rett and Cox, 2008). Larger poultry population sizes and densities facilitategreater transmission. Such crowded conditions depress immune response. Highturnover, a part of any industrial production, provides a continually renewedsupply of susceptibles, the fuel for the evolution of virulence.

There are additional pressures on influenza virulence on such farms. Assoon as industrial poultry reach the right bulk they are killed. Think ‘NoFactory for Old Chickens,’ with Javier Bardem as the plant manager. Resi-dent influenza infections must reach their transmission threshold quickly inany given bird, before the chicken or duck or goose is sacrificed. The quickerviruses are produced, the greater the damage to the chicken. Increasing age-specific mortality in factory chickens should select for greater virulence. Withinnovations in production the age at which chickens are processed has been re-duced from 60 days to 40 days (Striffler, 2005), increasing pressure on virusesto reach their transmission threshold – and virulence load – that much faster.

Along with hosting experiments in mounting virulence, industrial produc-tion has also increased the diversity of human-friendly influenza. Over the past15 years an unprecedented variety of influenzas capable of infecting humanshas emerged across the global archipelago of factory farms. Along with H5N1there are H7N1, H7N3, H7N7, H9N2, in all likelihood H5N2, and perhaps evensome of the H6 serotypes (WHO 2005, Puzelli et al. 2005, Meyers et al., 2007;Ogata et al., 2008). Something of a positive loop appears to have emerged inkind: the very efforts pursued to control pathogenic avian influenza may inpassing increase viral diversification. In late 2006, virologist Guan Yi and hiscolleagues at the University of Hong Kong identified the previously unchar-acterized Fujian-like H5N1 lineage (Smith et al., 2006). The team ascribedthe emergence of the strain as a viral evolutionary reaction to the Chinesegovernment’s campaign to vaccinate poultry. As in the case of other influenzaserotypes (Suarez et al., 2006; Escorcia et al., 2008), the virus appeared toevolve out from underneath the pressure of vaccine coverage.

Factory farms provide what seems to be an ideal environment for theevolution of a variety of virulent influenzas. And that seems to be a costagribusiness is willing to incur for the cheaper manufacture of its product.

6.4.3 The political virology of offshore farming

In Israel recently researchers selected for a lineage of featherless chickens(Yaron et al., 2004). The birds look like walking groceries, ready to hop upinto the meats freezer in aisle 6 of your local supermarket. These chickens,able to survive in warm climes alone, were developed in the interests of theproducer, not the consumer. Consumers have long avoided plucking feathers.That’s typically done at the factory. A featherless poultry will allow producers,on the other hand, to scratch off plucking feathers from production. The baldbird offers the anatomical equivalent of the factory epidemiology agribusinessis imposing on poultry-generating artificial chicken ecologies that could never


persist in nature because of the epidemiological costs they incur, but thatallow more poultry to be processed faster. The resulting costs are shifted toconsumers and taxpayers alike.

The lengths to which agribusiness has changed poultry production are re-markable, including, more recently, in the present avian influenza zone. South-ern China serves as a regional incubator for new methods in poultry breeding(Luo et al., 2003); Sun et al., (2007), for instance, describe a Guangdongprogram in which geese were exposed to a counter-seasonal lighting schedulethat induced out-of-season egg-laying. The innovation helped double profitsfor local goose production and expanded the market, and Chinese appetite,for goose meat. The resulting market advantages forced smaller farms out ofbusiness and led to a consolidation of the province’s agribusiness. The struc-tural shift marks a perverse turn back toward the farm collectivization theChinese government abandoned in 1980, this time, though, under the controlof far fewer hands.

Karl Marx (1867/1990) traced many of the fundamentals of such efforts atcommodification. In the first chapter of the first volume of Capital Marx wrotethat human-made objects have multiple characteristics. They have use value –a hammer can be used to beat down nails. In all human economies objects alsohave an exchange value-how many other objects (say, screwdrivers) for whicha hammer can be exchanged. A capitalist economy adds a third characteristic,turning objects into commodities. Surplus value is that part of the object’sworth that accrues to capitalists as profit. Marx’s contribution was showingthat capitalists expropriate the surplus value by taking it out of the valuethat workers added to the commodity when they make it, usually by payingworkers lower wages or increasing worker productivity, paying them the sameor less for more work.

In our efforts to better understand how influenza evolves we need onlyaddress here Marx’s point that capitalists produce commodities not becausecommodities are useful – have use value – but because they accrue surplusvalue, to capitalists the most important characteristic of the object. Changingthe color or style of a hammer to attract more consumers may not seem such abig deal, but for other objects changes in use value can have far-reaching, evendangerous, consequences. In this case, agribusiness has changed its commod-ity – living, breathing organisms-to maximize productivity. But what does itmean to change the use value of the creatures we eat? What happens whenchanging use value turns our poultry into plague carriers? Does out-of-seasongoose production, for instance, allow influenza strains to avoid seasonal extir-pation, typically a natural interruption in the evolution of virulence? Are theresulting profits defensible at such a cost to the rest of us?

Mass commodification of poultry emerged in what is now called the ‘Live-stock Revolution.’ Before the great shift, poultry was largely a backyard op-eration. In Boyd and Watts’ (1997) map of poultry across the United Statesin 1929, each dot represents 50,000 chickens. We see wide dispersion acrossthe country-300 million poultry total at an average flock size of only 70 chick-


ens. The production filiere of that era shows local hatcheries sold eggs tobackyard poultry producers and independent farmers, who in turn contractedindependent truckers to bring live poultry to city markets.

That changed after WWII. Tyson, Holly Farms, Perdue, and other com-panies vertically integrated the broiler filiere, buying up other local producersand putting all nodes of production under one company’s roof (Manning andBaines, 2004; Striffler, 2005). Boyd and Watts show by 1992 US poultry pro-duction is largely concentrated in the South and parts of a few other states.Each dot now represents 1 million broilers, 6 billion in total, with averageflock size of 30,000 birds.

By the 1970s, the new production model was so successful it was producingmore poultry than people typically ate. How many roasted chickens werefamilies prepared to eat a week? With the assistance of food science andmarketing the poultry industry repackaged chicken in a mind-boggling arrayof new products, including chicken nuggets, strips of chicken for salads, and catfood. Multiple markets were developed large enough to absorb the production.

Industrial poultry also spread geographically. With production widespread,world poultry meat increased from 13 million tons in the late 1960s to about62 million by the late 1990s, with the greatest future growth projected in Asia(FAO, 2003). In the 1970s Asian-based companies such as Charoen Pokphandset up vertical filieres in Thailand and, soon after, elsewhere in the region. In-deed, CP was the very first foreign company allowed to set up production inGuangdong under Deng Xiaoping’s economic reforms. China has since hosteda veritable explosion in annual chickens and ducks produced (Gilbert et al.,2007). Increases in poultry have also occurred throughout Southeast Asia,though not nearly at the magnitude of China.

According to geographer David Burch (2005), the shift in the geographyof poultry production has some very interesting consequences. Yes, agribusi-nesses are moving company operations to the Global South to take advantageof cheap labor, cheap land, weak regulation, and domestic production hob-bled in favor of heavily subsidized agro-exporting (Manning and Baines, 2004;McMichael, 2006). But companies are also engaging in sophisticated corpo-rate strategy. Agribusinesses are spreading their production line across muchof the world. For example, the CP Group, now the world’s fourth largest poul-try producer, has poultry facilities in Turkey, China, Malaysia, Indonesia, andthe US. It has feed operations across India, China, Indonesia, and Vietnam.It owns a variety of fast food chain restaurants throughout Southeast Asia.

Such rearrangements falsify the widely promulgated assumption that themarket corrects corporate inefficiencies. On the contrary, vertical multination-alism cushions companies from the consequences of their own mistakes. First,multinationals producing at scale can price unprotected local companies out ofbusiness – the Wal-Mart effect. Consumers have nowhere else to go to punishsubsequent corporate blunders. Secondly, by threatening to move operationsabroad multinationals can control local labor markets; hobbling unions, block-ing organization drives, and setting wages and working conditions. Unions are


an important check on production practices that affect not only workers andconsumers, but both directly and by proxy the animals involved in produc-tion. Thirdly, vertical agribusiness acts as both poultry supplier and retailer.The CP Group, for instance, owns a number of fast-food chains in a numberof countries selling, what else, CP chicken. In short, fewer independent chainsexist to play suppliers off each other by demanding the food be prepared in away healthy to animals and humans alike.

In operating factories across multiple countries multinationals can hedgetheir bets in a variant of David Harvey’s (1982/2006) spatial fix. The CPGroup operates joint-venture poultry facilities across China, producing 600million of China’s 2.2 billion chickens annually sold (Burch, 2005). When anoutbreak of avian influenza occurred in a farm operated by the CP Groupin Heilongjiang Province, Japan banned poultry from China. CP factories inThailand were able to take up the slack and increase exports to Japan. Withthe price per poultry ton increasing in the wake of an avian influenza crisis ithelped create, the CP Group grossed greater profits. A supply chain arrayedacross multiple countries increases the risk of avian influenza spread even asit allows some companies the means by which to compensate for the resultinginterruptions in business (Sanders, 1999; Manning et al., 2007).

To protect the interests of agribusiness even as its operations struggle orfail, multinationals also fund politicians or field their own candidates. ThaksinShinawatra, the Prime Minister of Thailand during the country’s first avianinfluenza outbreaks, came to power on the backs of the telecommunicationsand livestock industries. Shinawatra played a prime role in blocking Thaiefforts to control avian influenza. As Mike Davis (2005) describes it, whenoutbreaks began in Thailand, corporate chicken-processing plants acceleratedproduction. According to trade unionists processing increased at one factoryfrom 90,000 to 130,000 poultry daily, even as it was obvious many of the chick-ens were sick. As word got out about the illness, Thailand’s Deputy Ministerof Agriculture made vague allusions to an ‘avian cholera’ and Shinawatra andhis ministers publicly ate chicken in a show of confidence.

It later emerged that the CP Group and other large producers were collud-ing with government officials to pay off contract farmers to keep quiet abouttheir infected flocks. In turn, livestock officials secretly provided corporatefarmers vaccines. Independent farmers, on the other hand, were kept in thedark about the epidemic, and they and their flocks suffered for it. Once thecover-up was blown open, the Thai government called for a complete mod-ernization of the industry, including requiring all open-air flocks exposed tomigratory birds be culled in favor of new biosecure buildings only wealthierfarmers could afford.

Attempts to proactively change poultry production in the interests of stop-ping avian influenza can be met with severe resistance by governments be-holden to corporate sponsors. In effect, H5N1, by virtue of its associationwith agribusiness, has some of the most powerful representatives available


defending its interests in the halls of government. The very biology of avianinfluenza is enmeshed with the political economy of the business of food.

If multinational agribusinesses can parlay the geography of productioninto huge profits, regardless of the outbreaks that may accrue, who pays thecosts? The costs of factory farms have long been externalized. As Peter Singer(2005) explains, the state has been forced to pick up the tab for the problemsthese factories cause; among them, health problems for its workers, pollutionreleased into the surrounding land, food poisoning, and damage to transporta-tion infrastructure. A breach in a poultry lagoon, releasing a pool of poultryshit into a Cape Fear tributary that causes a massive fish kill, is left to localgovernments to clean up.

With the specter of avian influenza the state is again prepared to pick upthe bill so that farm factories can continue to operate without interruption,this time in the face of a worldwide pandemic agribusiness helped cause in thefirst place. The economics are startling. The world’s governments are preparedto subsidize agribusiness billions upon billions for damage control in the formof animal and human vaccines, Tamiflu, and body bags. Along with the livesof millions of people, the establishment appears willing to gamble much ofthe world’s economic productivity, which stands to suffer catastrophically ifa pandemic were to erupt.

6.4.4 Why Guangdong? Why 1997?

In reorganizing its poultry industry under the American model of verticallyintegrated farming, Chinese farming helped accelerate a phase change in in-fluenza ecology, selecting for strains of greater virulence, wider host range, andgreater diversity. For decades a variety of influenza subtypes have been dis-covered emanating from southern China, Guangdong included (Chang, 1969;Shortridge and Stuart-Harris, 1982; Xu et al., 2007; Cheung et al., 2007). Inthe early 1980s, with poultry intensification under way, University of HongKong microbiologist Kennedy Shortridge (1982) identified 46 of the 108 dif-ferent possible combinations of hemagglutinin and neuraminidase subtypescirculating worldwide at that time in a single Hong Kong poultry factory.

Shortridge detailed the likely reasons southern China would serve asground zero for the next influenza pandemic:

[1] Southern China hosts mass production of ducks on innumerable ponds,facilitating fecal-oral transmission of multiple influenza subtypes.

[2] The greater mix of influenza serotypes in southern China increases thepossibility the correct combination of gene segments would arise by geneticreassortment, selecting for a newly emergent human strain.

[3] Influenza circulates year-round there, surviving the interepidemic pe-riod by transmitting by the fecal-oral mode of infection.

[4] The proximity of human habitation in southern China provides an idealinterface across which a human-specific strain may emerge.


The conditions Shortridge outlined twenty-five years ago have since onlyintensified with China’s liberalizing economy. Millions of people have movedinto Guangdong the past decade, a part of one of the greatest migration eventsin human history, from rural China into cities of the coastal provinces (Fan,2005). Shenzhen, one of Guangdong’s Special Economic Zones for open trade,grew from a small city of 337,000 in 1979 to a metropolis of 8.5 million by2006. As discussed earlier, concomitant changes in agricultural technologyand ownership structure have put hundreds of millions more poultry intoproduction (Luo et al., 2003; Burch, 2005; Sun et al., 2007). Poultry outputincreased in China from 1.6 million tons in 1985 to nearly 13 million tons by2000.

As Mike Davis (2005) summarizes it, by the onset of pathogenic H5N1,only the latest pathogen to emerge under such socioecological conditions,

“[S]everal subtypes of influenza were traveling on the path towardpandemic potential. The industrialization of south China, perhaps,had altered crucial parameters in the already very complex ecologicalsystem, exponentially expanding the surface area of contact betweenavian and nonavian influenzas. As the rate of interspecies transmissionof influenza accelerated, so too did the evolution of protopandemicstrains.”

Pathogenic H5N1’s hemagglutinin protein was first identified by Chinesescientists from a 1996 outbreak on a goose farm in Guangdong (Tang et al.,1998). News reports during the initial H5N1 outbreak in Hong Kong detailedlocal health officials’ decision to ban poultry imports from Guangdong fromwhere several batches of infected chickens originated (Kang-Chung, 1997).Phylogeographic analyses of H5N1’s genetic code have pointed to Guang-dong’s role in the emergence of the first and subsequent strains of pathogenicH5N1 (Wallace et al., 2007). Scientists from Guangdong’s own South ChinaAgricultural University contributed to a 2005 report showing that a new H5N1genotype arose in western Guangdong in 2003-4 (Wan et al., 2005).

Subsequent work has complicated the picture. With additional H5N1 sam-ples from around southern China, Wang et al. (2008) showed virus from thefirst outbreaks in Thailand, Vietnam and Malaysia appeared most related toisolates from Yunnan, another southern Chinese province. Indonesia’s out-breaks were likely seeded by strains isolated from the province of Hunan.These are important results, showing the complexity of influenza’s landscape.At the same time they need not absolve Guangdong. Even if some H5N1strains emerged elsewhere in the region, Guangdong’s socioeconomic central-ity may have acted as an epidemiological attractant, drawing in novel poultrytrade-borne strains from around southern China before dispersing them againback out across China and beyond.

Mukhtar et al. (2007) meanwhile traced the origins of the genomic seg-ments from the original 1996 outbreak in Guangdong. Most of the internalproteins (encoding for proteins other than surface proteins hemagglutinin and


neuraminidase) appeared phylogenetically closest to those of H3N8 and H7N1isolates sampled from Nanchang in nearby Jiangxi Province. The 1996 hemag-glutinin and neuraminidase appeared closest to those of H5N3 and H1N1 iso-lates from Japan. In the months before the outbreak in Hong Kong severalof the proteins were again replaced by way of recombination, this time viastrains of H9N2 and H6N1 (Guan et al., 1999; Hoffmann et al., 2000). H5N1outbreaks in the years that followed Hong Kong emerged by still more re-combination (Li et al., 2004). The sociogeographic mechanisms by which thevarious segments first converged (and were repeatedly shuffled) in Guangdongremain to be better outlined. The results so far do indicate the spatial expanseover which reassortants originate may be greater than Kennedy Shortridge,or anyone else, previously outlined. But genomic origins tell us little how thisparticular complement led to a virus that locally evolved such virulence otherthan showing the genetic variation upon which the virus can draw.

A closer look at Guangdong’s drastically shifting socioeconomic circum-stances, then, appears necessary in better illuminating the local conditionsthat selected for such deadly pathogens so easily spread; not only H5N1, buta diverse viral portfolio, including influenza A (H9N2) (Liu et al., 2003), H6N1(Cheung et al., 2007), and SARS (Poon et al., 2004). What exactly are the‘crucial parameters’ for the area’s disease ecosystem? What are the mecha-nisms by which changes in southern China’s human-animal composite lead toregular viral pulses emanating out to the rest of China and the world? WhyGuangdong? Why 1997 and thereafter?

6.4.5 700 million chickens

We begin with the death of Mao and the rehabilitation of Deng Xiaoping.In the late 1970s, China began to move away from a Cultural Revolutionpolicy of self-sufficiency, in which each province was expected to produce mostfoods and goods for its own use. In its place, the central government beganan experiment centered about a reengagement with international trade inSpecial Economic Zones set up in parts of Guangdong (near Hong Kong)and Fujian (across from Taiwan), and later the whole of Hainan Province.In 1984, 14 coastal cities-including Guangzhou and Zhanjiang in Guangdong-were opened up as well although not to the extent of the economic zones(Tseng and Zebregs, 2003).

By macroeconomic indicators favored by establishment economists, thepolicy was a success. Between 1978 and 1993 China’s trade-to-GNP ratiogrew from 9.7% to 38.2% (Perkins, 1997). Most of this growth stemmed frommanufactured goods produced by foreign-funded joint ventures and townshipand village enterprises (TVE) allowed greater autonomy from central control.Foreign direct investment (FDI) increased from nothing to US $45 billion bythe late 1990s, with China the second greatest recipient after the US. Sixtypercent of the FDI was directed to cheap-labor Chinese manufacturing. Given


the extent of China’s small-holder farming, little FDI was initially directed toagriculture (Rozelle et al., 1999).

That has since begun to change. Through the 1990s poultry productiongrew at a remarkable 7% per year (Hertel et al., 1999). Processed poultry ex-ports grew from US $6 million in 1992 to US$774 million by 1996 (Carter andLi, 1999). The Interim Provisions on Guiding Foreign Investment Direction,revised in 1997, aim to encourage FDI across a greater expanse of China andin specific industries, agriculture included (Tseng and Zebregs, 2003). China’slatest 5-year plan sets sights on modernizing agriculture nationwide (Tan andKnor, 2006). Since China joined the WTO in 2002, with greater obligations toliberalize trade and investment, agricultural FDI has doubled (Whalley andXin, 2006). But much opportunity for AgFDI remains available to a widerarray of sources of investment. By the late 1990s, Hong Kong and Taiwan’scontribution to China’s FDI had declined to 50% of the total, marking aninflux of new European, Japanese, and American investment.

In something of a bellwether, in August, 2008, days before the Olympics,U.S. private equity investment firm Goldman Sachs bought ten poultry farmsin Hunan and Fujian for US$300 million (Yeung, 2008). Although the imageof a band of New York brokers knee-deep in chicken shit may prompt a cackle,Goldman Sachs has contracted third parties to run the farms. The outrightownership appears a step beyond the joint ventures in which Goldman Sachshad until then participated. Goldman Sachs already holds a minority stakein Hong Kong-listed China Yurun Food Group, a mainland meat productsmanufacturer, and 60% of Shanghai-listed Shuanghui Investment and Devel-opment, another meat packer. Goldman Sachs’ new purchase, further up thefiliere, signals a shift in the global fiscal environment. The firm has voted withits feet, deftly moving out of high-risk US mortgages and, during a global foodcrisis, into Chinese farming.

Guangdong remains at the cutting edge of the economic shift. It hostedthe central government’s first efforts at internationalizing the rural economy(Zweig, 1991; Johnson, 1992; Xueqiang et al., 1995). Starting in 1978, agricul-tural production was redirected from domestic grain to Hong Kong’s market.Hong Kong businesses invested in equipment in return for new output in veg-etables, fruit, fish, flowers, poultry and pig. In something of a return to itshistorical role, Hong Kong (‘the front of the store’) also offered Guangdong(‘the back of the store’) marketing services and access to the internationalmarket (Sit, 2004; Heartfield, 2005). In a few short years Guangdong’s econ-omy again became entwined with and dependent upon Hong Kong’s economicfortunes. And vice versa. As of the Hong Kong outbreak, investment in Chinacomprised 4/5 of Hong Kong’s FDI outflow (Heartfield, 2005). Much of HongKong-funded production is now conducted in Guangdong, with Hong Kong’sindustrial base increasingly hollowed out as a result.

Eighty-five percent of the agricultural FDI brought in during the 1990s wasfunneled into Guangdong and several of the other coastal provinces (Rozelleet al., 1999). Guangdong was allowed to invest more in its transportation


infrastructure, an invitation for further investment. Many of the province’scompanies were allowed to claim 100% duty drawbacks. Guangdong also de-veloped trading arrangements with many of the 51 million Chinese overseas(Gu et al. 2001, Heartfield 2005). As a class the expatriates, nearly 200 yearsabroad, control large percentages of regional market capital, including in In-donesia, Thailand, Vietnam, the Philippines, Malaysia, and Singapore. At thetime of the first H5N1 outbreaks overseas Chinese collectively comprised thegroup with the greatest investment in mainland China (Haley et al. 1998).

As a result of the area-specific liberalization, Guangdong accounted for42% of China’s total 1997 exports and generated China’s largest provincialGDP (Lin, 2000; Gu et al., 2001). Of the coastal provinces, Guangdong hostedthe greatest concentration of joint-venture export-oriented firms, with the low-est domestic costs for each net dollar of export income (Perkins 1997). Guang-dong’s three free economic zones (Shenzhen, Shantou and Zhuhai) boasted anexport-to-GDP ratio of 67%, compared to a national average of 17%.

By 1997, and the first H5N1 outbreak in Hong Kong, Guangdong, hometo 700 million chickens, served as one of China’s top three provinces in poul-try production (Organisation for Economic Co-operation and Development,1998). Fourteen percent of China’s farms with 10,000 or more broilers werelocated in Guangdong (Simpson et al., 1999). Guangdong’s poultry operationswere by this point technically modernized for breeding, raising, slaughtering,and processing birds, and vertically integrated with feed mills and processingplants. AgFDI helped import grandparent genetic stock, support domesticbreeding, and introduce superior nutrition feed milling/mixing (Rozelle et al.,1999). Production has been somewhat constrained by access to interprovincialgrain and the domestic market’s preference for native poultry breeds less ef-ficient at converting feed. Of obvious relevance, production also suffered frominadequate animal health practices.

The rate and magnitude of poultry intensification poultry appears to havecombined with the pressures placed on Guangdong wetlands by industry anda burgeoning human population to squeeze a diversifying array of influenzaserotypes circulating year-round through something of a virulence filter. Theresulting viral crop-for 1997, H5N1 by molecular happenstance-is exportedout by easy access to international trade facilitated in part by expatriatecompanies.

Guangdong’s ascension wasn’t without its detractors. Domestic produc-ers in Hong Kong competed with Hong Kong-Guangdong joint ventures forexport licenses (Zweig, 1991). Landlocked provinces meanwhile chafed at theliberalization the central government proffered coastal provinces alone. Withso much domestic currency on hand, the coastal provinces could outcom-pete inland provinces for livestock and grain produced by the inland’s ownTVEs. The coastal provinces were able to cycle their competitive advantageby turning cheap grain into more profitable poultry or flat-out re-exportingthe inland goods, accumulating still greater financial reserves. At one pointrivalries became so intense that Hunan and Guangxi imposed trade barriers


upon interprovincial trade. The central government’s efforts to negotiate in-terprovincial rivalries included spreading liberalization inland (Tan and Khor,2006). Provinces other than Guangdong and Fujian began to become entrainedinto market agriculture, albeit at a magnitude still outpaced by their coastalcounterparts. Industrial poultry’s expanding extent increases the geographicscope for H5N1’s emergence and may explain the roles Yunnan and Hunanappear to have played in serving up H5N1 abroad.

An additional source of conflict, often forgotten in the cacophony ofmacroeconomic indicators, requires comment-the Chinese people themselves.China’s state capitalism has induced such a polarization of wealth that, alongwith threatening its own economic growth, impoverishes hundreds of millionsof Chinese. In engaging in internally imposed structural adjustment Chinahas largely turned away from its real and ideological investment in the healthand wellbeing of its population (Hart-Landsberg and Burkett, 2005a). Tensof millions of state industrial workers have been laid off. Labor income as ashare of Chinese GDP fell from about 50% in the 1980s to under 40% by 2000(Li, 2008). FDI and private companies-under no obligation to offer housing,healthcare, or retirement benefits-are used to discipline Chinese workers whowere long used to a living wage, basic benefits, and job protections (Hart-Landsberg and Burkett, 2005b). Discipline, however, does not always take.Protests running now into the tens of thousands, some turning into riots re-quiring army deployment, have battered provincial governments accused ofcorruption, land confiscation, expropriating state assets, wage theft, and pol-lution. In something of an ironic twist, in defending foreign capital againstits own people China’s communist leadership has taken on the role of thecomprador class it defeated in 1949 (Heartfield, 2005).

Farmers have been particularly hard hit by the government’s capital-ist turn. While decollectivization of agricultural land to household controlpropped up by governmental price supports led to a doubling in rural in-comes by 1984, rural infrastructure and attendant social support deteriorated(Hart-Landsberg and Burkett, 2005a). In the late 80s, agricultural incomesstagnated, eaten away by inflation and a decline in price supports. Familiesbegan to abandon farming for informal industrial work in the cities. There,many rural migrants are treated as a reviled caste, discrimination codifiedby levels of officially designated migrant status and with attendant effects onincome (Fan 2001). China’s macroeconomic growth has been unable to absorbmany of the 100 million migrants.

Urbanization meanwhile has diffused out to the rural regions, eating uppeasant land. One million Chinese hectares have been converted from agri-culture to urban use (Davis, 2006). Remote sensing shows from 1990 to 199613% of agricultural land in a ten-county region in Guangdong’s Pearl Riverdelta was converted into non-agricultural use, in all likelihood China’s mostrapid conversion (Seto et al., 2000). Rural towns have been transformed intogrowing industrial cities, some supporting populations tipping a million people(Lin, 1997).


The termination of the commune system has left hundreds of millionsof peasants without access to medical care and health insurance (Shi 1993).Universal health coverage has degraded to 21% of the rural population insured(French, 2006). The number of affordable doctors has precipitously declined.Infant mortality has risen across many provinces. Rural public health haslargely collapsed. Hepatitis and TB are now widespread. HIV incidence hasincreased in several southeastern provinces, Guangdong included (Tucker etal., 2005). STI incidence by province is correlated with immigration associatedwith surplus men from rural regions separated from their families. Multitudesof malnourished and immunologically stressed peasants cycle-migrating backand forth from what may be the geographic origins of an influenza pandemicwould appear to compromise World Health Organization plans for interveningat any new infection’s source.

6.4.6 Asian financial flu

It is hard to talk of 1997 without mentioning two events of geopolitical signif-icance. On July 1 Hong Kong, long a British colony, was officially transferredto China as a Special Administrative Region, the first in a series of steps tofull integration to be undertaken up through 2047. The next day the Bank ofThailand floated the baht off the US dollar. The baht had been hammered bycurrency speculation and a crippling foreign debt. International finance fledthe baht and soon, with the economic strength of Thailand’s neighbors also un-der suspicion, from other regional currencies. The FDI-dependent economiesof the Philippines, Malaysia, Indonesia, Taiwan, and South Korea suffered inthe ensuing wave of devaluation. The rest of the world too felt the effectsof the infectious ‘Asian flu,’ as the crisis came to be called, with stock mar-kets worldwide free-falling in response. Although the transfer of Hong Kongto China and the Asian financial crisis followed the first outbreaks of avianinfluenza in March, the events marked long-brewing shifts in regional politicaleconomy with apparent impact on viral evolution and spread.

Hong Kong’s role in China’s internally imposed structural adjustment, aswe explored above, is amply documented. The intensification of Guangdongpoultry went hand in hand with the ongoing transformation of the province’sborder with Hong Kong (Breitung 2002). The resulting poultry traffic, how-ever, is in no way unidirectional. Hong Kong exports to mainland China largeamounts of poultry, fruits, vegetables, nuts, oilseeds, and cotton (Carter andLi 1999). There is too a large illegal trade. At the time of the outbreak, HongKong chicken parts smuggled into China alone may have amounted to overUS$300 million per year (USTR, 1998; Carter and Li, 1999). Hong Kong isclearly less a victim of Guangdong’s avian influenza ecology, as often por-trayed, than a willing participant.

Meanwhile, the financial crisis slowed China’s economy. But because ofthe central government’s intervention China avoided the worst of the flu (Lin,2000). By staking billions in public works and loans, China kept the economic


engine primed in the face of slowing exports. Prophetically, four years previ-ous, the central government introduced fiscal austerity measures to cool offinflation and the possibility of an overheated economy. An associated regula-tion package was initiated to control the kind of short-term speculation thatwould soon strain China’s regional neighbors. The central state maintainstight control over the macroeconomy, capital flows, and corporate structureeven as it cedes much of the day-to-day operations to provincial authorities.Concomitantly, China’s economy is more than export-driven. Even as aus-terity leaves millions of Chinese destitute in its wake (Hart-Landsberg andBurkett, 2005), the domestic economy continues to grow, albeit increasinglydependent on luxury goods and real estate speculation. Finally, exports outof China were until the crisis largely destined for East and Southeast Asia.During the crisis’ aftermath China redirected more of its trade to Europe,North America, Africa, Latin America, and Oceania. China, then, was ableto maintain a trade surplus, retain foreign investment, and prop the yuanagainst the fiscal buffet from abroad.

At the same time, China was something more than a bystander to thecrisis. Its economy’s growing size and hemispheric reach may have exposed itsneighbors to the worst excesses of the neoliberal model (Hart-Landsberg andBurkett, 2005a; Tan and Khor, 2006). In attracting FDI at rates above andbeyond those of its neighbors, China has become the prime exporter in theregion: textiles, apparel, household goods, televisions, desktop computers, anincreasing array of high-end electronics-you name it. The smaller economiesare forced to restructure production in such a way as to complement China’sincreasingly diverse commodity output, in a type of regional division-of-labor.China’s transnational impact on supply lines forces each country to dependon producing a smaller array of parts to be put together in China for finalexport.

The resulting economies are more dependent on what few foreign multi-nationals they are able to attract. The company town becomes the companycountry. Such economies are more ‘brittle’-less robust in reacting to and re-orienting around downturns in any single industry, a particularly perniciousproblem as the US begins to falter in its role of importer of last resort. Thecapital flight exposes countries to the temptations of currency speculation. Toattract additional investment, establishment economists declare these coun-tries, once burned by such speculation, must now remove remaining barriersto the movement of money, goods, and capital, leaving domestic productionunprotected, the very conditions that brought about the 1997 crisis in thefirst place.

It would appear bird flu and the financial flu are intimately connected,their relationship extending beyond serendipitous analogy. Although agricul-ture has until recently been less export-dependent than manufacturing, in partfrom its perishability and now endangered trade protections (Hertel et al.,2000), there are already a number of epidemiological ramifications. These in-clude a geographically expanding and intensifying poultry production, greater


exposure to transnational poultry, wider illegal poultry trade, and a truncationin animal health infrastructure by austerity measures domestically imposedin return for international loans (Rweyemamu et al., 2000). More acutely, theaftermath of the financial flu may have also provided China a window forexpanding regional poultry exports. A hypothesis worth testing is that someof these shipments seeded avian influenza outbreaks abroad.

How do we operationalize this model? How do we determine whethertransnational companies breed and spread avian influenza? Identifying poul-try crates carrying H5N1 country-to-country remains a difficult, but impor-tant, task (Kilpatrick et al., 2006). Tracing pathogens through commoditychains is increasingly an important topic of study and mode of intervention(Duffy et al., 2008). One difficulty centers about the willingness of govern-ment regulators to inspect poultry plants, including conditions under whichpathogen virulence may evolve. At the same time, there is a danger such ef-forts, once successful, may detract from the larger political ecology that shapesavian influenza evolution. With billions annually at stake, a few unlucky con-tract farmers or truck drivers may be sacrificed to protect a system stretchingacross a hemisphere’s interlocking markets. We’ve explored here the possibil-ity a deadly avian influenza is an unintended but not unexpected accessoryto multinational efforts to export a growing portfolio of Chinese agriculturalcommodities. The problem of avian influenza is more than a police matter. Itis systemic, buried deep in political tissue.

6.4.7 Layers of complication

Ending poultry production as we know it could make a great difference inGuangdong as elsewhere. But there are additional layers of complication.There is no easy one-to-one relationship between poultry density and H5N1outbreak at a variety of spatial scales. Across Asia, some areas where out-breaks have occurred support comparatively few poultry, while other areaswith millions of chickens have been so far left untouched. There is somethingof a stochastic component to disease spread. Epidemics start somewhere, inthis case in southern China, and take time to wend their way elsewhere, start-ing with regions nearby and, in part by due cause and in part by chance,farther abroad. There are, however, demonstrable causes other than thoseinside the poultry industry.

Thailand offers one such example. As mapped by ecologist Marius Gilbertand colleagues (Gilbert et al., 2006; Gilbert et al., 2008), the distribution ofThai broilers and backyard poultry appear little associated with H5N1 out-breaks. Local outbreaks appear better fitted to the densities of ducks thatare allowed to graze freely outside. After harvests these ducks are broughtin to feed on the rice that is left over on the ground. Satellite pictures showrice harvests matching duck densities. The more annual rice crops, the moreducks (and the greater the association with H5N1 outbreaks). It seems theseducks, free to graze outdoors, exposed to migratory birds, and tolerant of


a wider range of influenzas, serve as epidemiological conduits for infectingnearby poultry. While a rather ingenious agricultural practice, raising a co-hort of ducks on fallen waste rice may carry serious epidemiological overhead.Double- and even triple-cropping is practiced in other avian influenza zones,including southeastern China, the final stretches of the Xun Xi River, theGanges floodplain, and on the island of Java (Leff et al., 2004).

We have, then, an integrated viral ecology with highly complex dependen-cies. The variety of farming practices, for one, splits a-twain a number of faciledichotomies. There is a panoply of farm types, beyond the rough polarities of‘small’ and ‘large.’ In Thailand alone there are closed-off farms, open struc-tures with netting to block passerine birds, the aforementioned free-grazingducks, and backyard poultry (Songserm et al., 2006).

Even then, such a taxonomy implies a compartmentalization often absentin the field. On a recent trip to Lake Poyang in Jiangxi Province, China, a teamof international experts discovered an astonishing farming ecology in whichdomesticated free-range ducks fed in fields, bathed in local estuaries, swamin the lake, and intermingled and presumably interbred with wild waterfowl.Some flocks daily commuted across dikes from their sheds to the open waterand back. The epidemiological implications are obvious. Indeed, the facility bywhich pathogens spread and evolve in the area is of an order that, accordingto local farmers, chickens cannot be raised around the lake. For some poultryspecies the region is epidemiologically radioactive.

Absent too from the taxonomy are profound structural changes imposedby economic pressures upon world farming (Weis, 2007). For the past threedecades, the International Monetary Fund and the World Bank have madeloans to poorer countries conditioned on removing supports for domestic foodmarkets. Small farmers cannot compete with cheaper corporate imports subsi-dized by the Global North. Many farmers either give up for a life on periurbanmargins or are forced to contract out their services-their land, their labor-tolivestock multinationals now free to move in (Manning and Baines, 2004;Lewontin, 2007). The World Trade Organization’s Trade-Related InvestmentMeasures permit foreign companies, aiming to reduce production costs, to pur-chase and consolidate small producers in poorer countries (McMichael, 2006).Under contract, small farmers must purchase transnational-approved suppliesand are given no guarantee their birds will be bought back by their transna-tional partner. The new arrangements belie the superficial distinction thathas been made between factory farms exercising ‘biosecurity’ on the one handand small farmers whose flocks are exposed to the epidemiological elements.Factory farms ship day-old chicks to be raised piecework by small farmers.Once grown (and exposed to migratory birds), the grown birds are shippedback to the factory for processing. The violation of ‘biosecurity’ appears builtdirectly into the industrial model.

A third complication is the historical shift in the relationship betweennature and farming. Maps in Phongpaichit and Baker (1995) show since 1840Thailand has been transformed from primary wilderness into an agricultural


state, a veritable bread-basket. Agriculture’s new girth comes at the expense ofwetlands worldwide, either out-and-out destroyed, polluted, or irrigated dry.The latter abuse serves as another basis for conflicts between agribusiness andsmall farmers. Socially stratified power struggles over the Chao Phraya basinhave wracked Thailand for hundreds of years (Molle, 2007).

Wetlands have traditionally served as Anatidae migration pit stops (Lemlyet al., 2000). A growing literature shows many migratory birds are no sittingducks and have responded to the destruction of their natural habitat. Geese,for example, display an alarming behavioral plasticity, adopting entirely newmigratory patterns and nesting in new types of wintering grounds, movingfrom deteriorating wetlands to food-filled farms. The shift has for some popu-lations substantially increased their numbers (Jeffries et al. 2004, Van Eerdenet al., 2005). The population explosions have initiated a destructive feedbackin which the swarms of farm-fed migratory birds overgraze their Arctic breed-ing grounds to the point the tundra is transformed into a mud pit. In thecourse of colonizing our planet’s natural habitats-some 40% of the world’susable land now supports agriculture-we may have unintentionally expandedthe interface between migratory birds and domestic poultry.

Clearly agribusiness, structural adjustment, environmental destruction,climate change, and the emergence of avian influenza are more tightly in-tegrated than previously thought.

6.4.8 The political will for an epidemiological way?

Guangdong may only represent the front of a socioecological transformationspreading across much of southern China, as well as across much of the pop-ulated world. The origins of highly pathogenic H5N1 are multifactorial, withmany countries and industries and sources of environmental damage at fault.Can we then place blame on the country, say, Indonesia or Vietnam or Nige-ria, from which a human-to-human pandemic might first emerge? Should weblame China for repeatedly seeding outbreaks regionally and internationally?Should we blame Hong Kong for offshore farming? Or should we blame theUnited States, where the industrial model of vertically integrated poultry firstoriginated, with thousands of birds packed in as so much food for flu? Theanswers are yes, yes, yes, and yes. Blame, much as the problem itself, mustbe distributed about its multiple levels of social and ecological organization.

To break avian influenza’s back, or at the very least promote some sort ofsustainable epidemiological mitigation, a number of radically invasive changesare required, changes that challenge core premises of present political econ-omy, neoliberal and state capitalist alike. Whether there exists the politicalwill to change is an open question. Denial, jockeying, and obfuscation arepresently rampant. Chinese officials have expended much effort in flat-outdenying responsibility for avian influenza (Wallace, 2007) or, in the epidemio-logical equivalent of the American practice of paying off the families of collat-eral damage without admitting guilt, offering small sums to affected countries.


In 2007, China donated US $500,000 to Nigeria’s effort to fight avian influenza.Never mind that Nigeria would never have needed the aid if China hadn’t in-fected it with avian influenza in the first place. The Qinghai-like strain Nigerianow hosts first originated in southern China. Meanwhile, the US and EU, lay-ing undue blame on a stubborn Indonesia unwilling to share H5N1 samples,have blocked efforts to reform a system of worldwide vaccine production thatrewards pharmaceutical companies and the richest populations at the expenseof the poorest (Hammond, 2007, 2008).

What must be done to stop avian influenza, if the political will is foundby, or forced upon, governments worldwide? In the short term, small farmersmust be fairly compensated for poultry culled in an effort to control outbreaks.Poultry trade must be better regulated at international borders (Kilpatricket al., 2006; Wallace and Fitch, 2008). The world’s poor must be providedepidemiological assistance, as well as vaccine and antiviral at no cost (Cristalliand Capua, 2007; Ferguson 2007). Structural adjustment programs degradinganimal health infrastructure in the poorest countries must be terminated.

For the long term, we must end the poultry industry as we know it. Avianinfluenza now emerges by way of a globalized network of corporate poul-try production and trade, wherever specific strains first evolve. With poultrybatches whisked from region to region-transforming spatial distance into just-in-time expediency (Harvey, 1982/2006)-multiple strains of avian influenzaare continually introduced into localities filled with populations of susceptiblebirds. Such domino exposure serves as the fuel for the evolution of viral viru-lence. In overlapping each other along the links of agribusiness’s transnationalsupply chains, strains of avian influenza also increase the likelihood they canexchange genomic segments to produce a recombinant of pandemic potential.In addition to the petroleum wasted and the loss of local food sovereigntythere are epidemiological costs to the geometric increase in food miles.

We must instead devolve much of the production to regulated networksof locally owned farms. While the argument has been made that corporatechicken supplies the cheap protein many of the poorest need, the millions ofsmall farmers who feed themselves (and many millions more) would neverhave needed such a supply if they hadn’t been pushed off their lands in thefirst place. A reversal need not be solely an anachronistic turn to the smallfamily farm, but can include domestically protected farming at multiple scales(Levins, 1993, 2007; Brown and Getz, 2008). Farm ownership, infrastructure,working conditions, and animal health are inextricably linked. Once workershave a stake in both input and output-the latter by outright ownership, profitsharing, or the food itself-production can be structured in such a way thatrespects human welfare, and, as a consequence, animal health. With localfarming, genetic monocultures of domesticated bird which promote the evolu-tion of virulence can be diversified back into heirloom varieties that serve asimmunological firebreaks. The economic losses bird flu imposes upon globalpoultry can be tempered: fewer interruptions, eradication campaigns, pricejolts, emergency vaccinations, and wholesale flock repopulations (Van Assel-


donk et al., 2006). Rather than jury-rigged with each outbreak, restrictionson bird movement are built naturally into the independent farm model.

The devil of such a domain shift is in its details. Richard Levins (2007),with decades experience collaborating with local researchers and practitionerson ecological approaches to Cuban agriculture and public health, summarizessome of the many adjustments a new agriculture may require,

“Instead of having to decide between large-scale industrial typeproduction and a ”small is beautiful” approach a priori, we saw thescale of agriculture as dependent on natural and social conditions,with the units of planning embracing many units of production. Dif-ferent scales of farming would be adjusted to the watershed, climaticzones and topography, population density, distribution of availableresources, and the mobility of pests and their enemies.

The random patchwork of peasant agriculture, constrained by landtenure, and the harsh destructive landscapes of industrial farmingwould both be replaced by a planned mosaic of land uses in which eachpatch contributes its own products but also assists the production ofother patches: forests give lumber, fuel, fruit, nuts, and honey butalso regulate the flow of water, modulate the climate to a distanceabout ten times the height of the trees, create a special microclimatedownwind from the edge, offer shade for livestock and the workers, andprovide a home to the natural enemies of pests and the pollinators ofcrops. There would no longer be specialized farms producing only onething. Mixed enterprises would allow for recycling, a more diverse dietfor the farmers, and a hedge against climatic surprises. It would havea more uniform demand for labor throughout the year.”

The scale and practice of agriculture must be flexibly integrated into theregion’s physical, social and epidemiological landscapes. At the same time, itneed be acknowledged that under such an arrangement not all parcels will beroutinely profitable. Whatever reductions in income farms accrue in protectingthe rest of the region must be offset by regular redistributive mechanisms(Richard Levins, personal communication).

Transforming the business of farming so broadly is likely only one of manysteps necessary to stop bird flu and other pathogens. For one, migratory birds,which serve as a fount of influenza strains, must concomitantly be weaned offagricultural land where they cross-infect poultry. To do so, wetlands world-wide, waterfowl’s natural habitat, must be restored. Global public health ca-pacity must also be rebuilt (Garrett, 2001). That capacity is only the mostimmediate bandage for the poverty, malnutrition, and other manifestationsof structural violence that promote the emergence and mortality of infectiousdiseases, including influenza (Kim et al., 2000; Farmer, 2004). Pandemic andinter-pandemic flu have the greatest impact on the poorest (Davis, 2005). Asfor many pathogens, particularly for such a contagious virus, a threat to oneis a threat to all.


Only once these objectives are fulfilled will we be able to better coverourselves against H5N1 and the other influenza serotypes now lining up likehurricanes brewing in the Atlantic.

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6 Farming human pathogens

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